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INS — INS
Pathways - manually collected, often from reviews:
-
BioCarta insulin signaling pathway:
Insulin/Insulin/Insulin Ra/Insulin Ra/Insulin Rb/Insulin Rb complex (INSR-INS)
→
Insulin (INS)
(modification, collaborate)
-
BioCarta growth hormone signaling pathway:
Insulin (INS)
→
Insulin/Insulin Ra/Insulin Ra/Insulin Rb/Insulin Rb complex (INS-INSR)
(modification, collaborate)
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insulin/IRS1 complex (INSR-INS-IRS1)
→
Insulin Receptor/Insulin/IRS1/NCK2 complex (INSR-INS-NCK2-IRS1)
(modification, collaborate)
Tu et al., Biochem J 2001*, Lee et al., Proc Natl Acad Sci U S A 1993
Evidence: physical interaction
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insuli/IRS1/GRB2/SHC complex (INSR-INS-SHC1-GRB2-IRS1)
→
Insulin Receptor/Insulin/IRS1 complex (INSR-INS-IRS1)
(modification, collaborate)
Wada et al., Endocrinology 1999, Sharma et al., Mol Endocrinol 2005, Kovacina et al., Biochem Biophys Res Commun 1993, Skolnik et al., Science 1993, Pronk et al., J Biol Chem 1993, Skolnik et al., EMBO J 1993, Ishihara et al., J Biol Chem 1997
Evidence: assay
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insulin/IRS1/Shp2 complex (INSR-INS-PTPN11-IRS1)
→
Insulin Receptor/Insulin/IRS1 complex (INSR-INS-IRS1)
(modification, collaborate)
Yamauchi et al., J Biol Chem 1995*
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insulin/SHC/GRB2/Sos1 complex (INSR-INS-SHC1-GRB2-SOS1)
→
Insulin Receptor/Insulin/SHC complex (INSR-INS-SHC1)
(modification, collaborate)
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insuli/IRS1/GRB2/SHC/PTP1B complex (INSR-INS-SHC1-GRB2-PTPN1-IRS1)
→
Insulin Receptor/Insulin complex (INSR-INS)
(modification, collaborate)
Hashimoto et al., J Biol Chem 1992, Hashimoto et al., Biochem J 1992, Kenner et al., J Biol Chem 1993
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insulin/SHC complex (INSR-INS-SHC1)
→
Insulin Receptor/Insulin/IRS1 complex (INSR-INS-IRS1)
(modification, collaborate)
Ozes et al., Proc Natl Acad Sci U S A 2001, Yamauchi et al., J Biol Chem 1994, Isakoff et al., J Biol Chem 1996*, Ishihara et al., J Biol Chem 1997
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insulin/SHC complex (INSR-INS-SHC1)
→
Insulin Receptor/Insulin complex (INSR-INS)
(modification, collaborate)
Ozes et al., Proc Natl Acad Sci U S A 2001, Yamauchi et al., J Biol Chem 1994, Isakoff et al., J Biol Chem 1996*, Ishihara et al., J Biol Chem 1997
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insulin/IRS1 complex (INSR-INS-IRS1)
→
Insulin Receptor/Insulin complex (INSR-INS)
(modification, collaborate)
Ozes et al., Proc Natl Acad Sci U S A 2001, Yamauchi et al., J Biol Chem 1994, Isakoff et al., J Biol Chem 1996*, Ishihara et al., J Biol Chem 1997
-
NCI Pathway Database Signaling events mediated by PTP1B:
Insulin Receptor/Insulin/SHC complex (INSR-INS-SHC1)
→
Insulin Receptor/Insulin/IRS1 complex (INSR-INS-IRS1)
(modification, collaborate)
Yamauchi et al., J Biol Chem 1994, Isakoff et al., J Biol Chem 1996*, Ishihara et al., J Biol Chem 1997
-
NCI Pathway Database Signaling events mediated by PTP1B:
Insulin Receptor/Insulin/SHC complex (INSR-INS-SHC1)
→
Insulin Receptor/Insulin complex (INSR-INS)
(modification, collaborate)
Yamauchi et al., J Biol Chem 1994, Isakoff et al., J Biol Chem 1996*, Ishihara et al., J Biol Chem 1997
-
NCI Pathway Database Signaling events mediated by PTP1B:
Insulin Receptor/Insulin/IRS1 complex (INSR-INS-IRS1)
→
Insulin Receptor/Insulin complex (INSR-INS)
(modification, collaborate)
Yamauchi et al., J Biol Chem 1994, Isakoff et al., J Biol Chem 1996*, Ishihara et al., J Biol Chem 1997
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insulin/IRS3 complex (INSR-INS)
→
Insulin Receptor/Insulin complex (INSR-INS)
(modification, collaborate)
Xu et al., J Biol Chem 1999*
Evidence: assay, physical interaction, other species
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insulin/SHC complex (INSR-INS-SHC1)
→
Insulin Receptor/Insulin/SHC/GRB10 complex (INSR-INS-SHC1-GRB10)
(modification, collaborate)
O'Neill et al., J Biol Chem 1996, Dong et al., Mol Endocrinol 1997*
Evidence: physical interaction
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insuli/IRS1/GRB2/SHC/Sos complex (INSR-INS-SHC1-SOS1-GRB2-IRS1)
→
Insulin Receptor/Insuli/IRS1/GRB2/SHC complex (INSR-INS-SHC1-GRB2-IRS1)
(modification, collaborate)
Pronk et al., Mol Cell Biol 1994
Evidence: assay, physical interaction
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insulin/SHC/GRB10 complex (INSR-INS-SHC1-GRB10)
→
Insulin Receptor/Insulin/SHC/GRB2/Sos1 complex (INSR-INS-SHC1-GRB2-SOS1)
(modification, inhibits)
Wick et al., J Biol Chem 2001
Evidence: assay
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insulin complex (INSR-INS)
→
Insulin (INS)
(modification, collaborate)
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insuli/IRS1/GRB2/SHC/PTP1B complex (INSR-INS-SHC1-GRB2-PTPN1-IRS1)
→
Insulin Receptor/Insuli/IRS1/GRB2/SHC complex (INSR-INS-SHC1-GRB2-IRS1)
(modification, collaborate)
Goldstein et al., J Biol Chem 2000, Dadke et al., J Biol Chem 2000, Seely et al., Diabetes 1996, Bandyopadhyay et al., J Biol Chem 1997
Evidence: mutant phenotype, assay
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insulin/GRB14/PDK1 complex (INSR-INS-GRB14-PDPK1)
→
Insulin Receptor/Insulin complex (INSR-INS)
(modification, collaborate)
King et al., J Biol Chem 2004*
Evidence: mutant phenotype, assay, physical interaction
-
Reactome Reaction:
INS
→
INS
(direct_complex)
-
Reactome Reaction:
INS
→
INS
(reaction)
Bouzakri et al., Cell Metab 2006, Kahn , Diabetes 1994*, White et al., J Biol Chem 1994*
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Bind Interaction:
INS
—
INS
Smith et al., Proc Natl Acad Sci U S A 1984*, Smith et al., Proc Natl Acad Sci U S A 1994*, Ciszak et al., Biochemistry 1994*, Ciszak et al., Structure 1995*
-
IRef Bind Interaction:
INS
—
INS
Yao et al., Acta Crystallogr D Biol Crystallogr 1999*
-
IRef Bind Interaction:
INS
—
INS
Jørgensen et al., J Mol Biol 1992*, Kristensen et al., J Mol Biol 1991*, Sørensen et al., Biochemistry 1994*
-
IRef Bind_translation Interaction:
INS
—
INS
(x-ray crystallography)
Smith et al., Proc Natl Acad Sci U S A 1984*
-
IRef Bind_translation Interaction:
INS
—
INS
(x-ray crystallography)
-
IRef Bind_translation Interaction:
INS
—
INS
(x-ray crystallography)
Ludvigsen et al., Biochemistry 1994*
-
IRef Bind_translation Interaction:
INS
—
INS
(x-ray crystallography)
-
IRef Bind_translation Interaction:
INS
—
INS
(x-ray crystallography)
Hua et al., Nature 1991*
-
IRef Bind_translation Interaction:
INS
—
INS
(x-ray crystallography)
Hua et al., Nature 1991*
-
IRef Bind_translation Interaction:
INS
—
INS
(x-ray crystallography)
-
IRef Bind_translation Interaction:
INS
—
INS
(x-ray crystallography)
Hua et al., Nature 1991*
-
IRef Bind_translation Interaction:
INS
—
INS
(x-ray crystallography)
Keller et al., Biochemistry 2001*
-
IRef Bind_translation Interaction:
INS
—
INS
(x-ray crystallography)
Tang et al., Biochemistry 1999*
-
IRef Bind_translation Interaction:
INS
—
INS
(x-ray crystallography)
Hua et al., J Mol Biol 1996*
-
IRef Dip Interaction:
INS
—
INS
(direct interaction, x ray scattering)
Vestergaard et al., PLoS Biol 2007*
-
IRef Dip Interaction:
INS
—
INS
(direct interaction, x-ray fiber diffraction)
Vestergaard et al., PLoS Biol 2007*
-
IRef Hprd Interaction:
INS
—
INS
(in vivo)
Air et al., Endocrinology 2002*
-
IRef Intact Interaction:
INS
—
INS
(direct interaction, blue native page)
Lind et al., FEBS J 2010*
-
IRef Intact Interaction:
INS
—
INS
(direct interaction, dynamic light scattering)
Lind et al., FEBS J 2010*
-
IRef Intact Interaction:
INS
—
INS
(direct interaction, nuclear magnetic resonance)
Lind et al., FEBS J 2010*
-
IRef Intact Interaction:
INS
—
INS
(direct interaction, fluorescence technology)
Lind et al., FEBS J 2010*
-
IRef Intact Interaction:
INS
—
INS
(direct interaction, circular dichroism)
Lind et al., FEBS J 2010*
-
IRef Intact Interaction:
INS
—
INS
(direct interaction, x-ray crystallography)
Tang et al., Biochemistry 1999*
-
IRef Intact Interaction:
INS
—
INS
(direct interaction, dynamic light scattering)
Landreh et al., FEBS J 2012*
-
IRef Intact Interaction:
INS
—
INS
(direct interaction, fluorescence technology)
Landreh et al., FEBS J 2012*
-
IRef Intact Interaction:
INS
—
INS
(direct interaction, molecular sieving)
Landreh et al., FEBS J 2012*
-
IRef Intact Interaction:
INS
—
INS
(direct interaction, fluorescence technology)
Nault et al., FEBS Lett 2013*
-
IRef Intact Interaction:
INS
—
INS
(direct interaction, atomic force microscopy)
Babenko et al., FEBS Lett 2013*
-
IRef Intact Interaction:
INS
—
INS
(direct interaction, circular dichroism)
Babenko et al., FEBS Lett 2013*
-
IRef Intact Interaction:
INS
—
INS
(direct interaction, x-ray crystallography)
Smith et al., Protein Sci 1996*
Text-mined interactions from Literome
Geffner et al., Lancet 1986 (Growth Disorders) :
Thyroid function, prolactin,
insulin response to oral glucose, glucose response to intravenous
insulin , and computerised tomography of the head were all normal
Hu et al., Diabetologia 2007 (Adenocarcinoma...) :
T33 is non-thiazolidinedione PPARalpha/gamma dual agonist which directly increases basal and insulin stimulated glucose uptake in adipocytes and secondarily improves
insulin action on
insulin signalling and glucose metabolism in skeletal muscle from diabetic ob/ob mice
Venieratos et al., Cell Signal 2010 :
Results showed that prolonged exposure of betaTC-6 cells to increased glucose concentrations resulted in significant inhibition of
insulin induced tyrosine phosphorylation of the
insulin receptor (IR) , and insulin receptor substrate-2 (IRS-2) as well as PI3-kinase activation
Stagner et al., J Clin Invest 1986 :
These results suggest that exogenous
insulin does not directly suppress the B cell, but can
suppress insulin secretion through an indirect neurally mediated, insulin dependent nerve mechanism
Verspohl et al., Acta Diabetol Lat 1982 :
In the perfused pancreas the inhibition concerned the first and the second phase of insulin release ; ( 2 ) the EC50 ( half-maximal inhibitory effect of insulin on glucose induced insulin secretion ) in islets was 1.2 nM ( = 160 microU/ml ) and 2.8 nM ( 390 microU/ml ) in perfused pancreas ; ( 3 ) exogenous
insulin also
inhibited insulin release in response to leucine and arginine in the isolated islet system and in the perfused pancreas ; ( 4 ) using aminophylline and tolbutamide in combination with glucose, the extent of the inhibitory effect of insulin was in the range of the inhibitory effect when glucose was used alone as stimulator in islets
Mulder et al., J Endocrinol 1997 (Diabetes Mellitus, Experimental) :
In contrast, insulin gene expression was the same at both time points in insulin treated rats, suggesting that
insulin impaired
insulin expression ... To summarize, we found that IAPP and
insulin were differentially expressed in experimental diabetes and that insulin treatment
inhibited insulin , but not IAPP, gene expression
Lennox et al., ChemMedChem 2013 (Insulin Resistance) :
GLP-1-Glu-PAL markedly decreased glycemic excursion following intraperitoneal glucose ( 32-48 % decrease, p < 0.05 ), enhanced
insulin response to glucose ( 2- to 2.3-fold, p < 0.05 to p < 0.01 ), and improved
insulin sensitivity ( 25-38 % decrease in plasma glucose, p < 0.05 )
Zabolotny et al., J Biol Chem 2004 (Insulin Resistance) :
Insulin stimulated
insulin receptor (IR) tyrosyl phosphorylation and phosphatidylinositol 3'-kinase activity were impaired by 35 % and 40-60 % in muscle of PTP1B overexpressing mice compared with controls
Pettersson et al., Peptides 1987 :
In summary, we have shown that GRP stimulates basal and potentiates stimulated
insulin and glucagon secretion in mice, and that the stimulatory effects of GRP on
insulin and glucagon secretion are partially
inhibited by muscarinic blockade by methylatropine or by beta-adrenoceptor blockade by propranolol
Barber et al., J Biol Chem 2001 :
SN50, a peptide inhibitor of NF-kappaB nuclear translocation, blocked the rescue effect of
insulin , but neither
insulin or serum deprivation
induced phosphorylation of IkappaB
Zethelius et al., Diabetes Care 2004 (Diabetes Mellitus, Type 2...) :
Insulin resistance, impaired early
insulin response , and insulin propeptides as predictors of the development of type 2 diabetes : a population based, 7-year follow-up study in 70-year-old men
Motley et al., Hypertension 2002 :
In addition, lysoPC inhibited the
insulin induced tyrosine phosphorylation of
insulin receptor substrate (IRS)-1 but not that of the insulin receptor beta subunit or insulin binding
Emanuelli et al., Diabetes 2004 (Insulinoma...) :
We show that IL-1beta decreases
insulin induced tyrosine phosphorylation of the insulin receptor (IR) and
insulin receptor substrate (IRS) proteins as well as phosphatidylinositol 3-kinase (PI3K) activation, and that this action is not due to the IL-1beta dependent nitric oxide ( NO ) production in RINm5F cells
Marshall et al., J Clin Invest 1980 (Insulin Resistance) :
In conclusion, ( a )
insulin leads to a dose dependent loss of
insulin receptors in freshly isolated adipocytes accompanied by the predicted functional consequence of decreased receptors, i.e., a rightward shift in the insulin-glucose transport dose-response curve, ( b ) prolonged incubation with insulin causes a marked postreceptor defect in the glucose transport system, ( c ) maintenance of the activated state of the glucose transport system prevents the expression of the post-receptor defect, ( d ) the location of the postreceptor abnormality is most likely in the glucose transport system per se, and ( e ) insulin induced receptor loss is accompanied by a decrease in insulin degradation
Echwald et al., Eur J Endocrinol 1999 :
Multiple regression analysis was employed to analyse the relationship between fasting serum leptin levels and levels of fasting serum insulin,
insulin sensitivity index and acute
insulin response ( AIR ) in a population based study of 380 young healthy Caucasians who underwent a combined intravenous glucose and tolbutamide tolerance test
Ogihara et al., Diabetes 2001 (Insulin Resistance) :
Interestingly, despite the presence of insulin resistance, high salt fed rats showed enhanced
insulin induced tyrosine phosphorylation of
insulin receptor substrate (IRS)-1 , IRS-2 ( liver and muscle ), and IRS-3 ( liver only ) ... Therefore, in both the liver and muscle of high salt fed rats, intracellular
insulin signaling leading to PI 3-kinase activation is enhanced and
insulin action is
attenuated
Novelli et al., Mol Cell Endocrinol 2004 (Diabetes Mellitus, Experimental...) :
The addition of L-NAME to control islets markedly
enhanced the
insulin response to arginine, as expected from the documented inhibitory effect exerted by nNOS activity in normal beta-cells, whereas it did not further modify the
insulin secretion in diabetic islets, thus implying the occurrence of a defective nNOS activity in these islets
Muniappan et al., BMC physiology 2007 :
Expression of either human
insulin or the beta cell specific transcription factors PDX-1, NeuroD1 and MafA in the Hepa1-6 cell line or primary liver cells via adenoviral gene transfer,
results in production and secretion of
insulin
Aspinwall et al., J Biol Chem 2000 :
Roles of insulin receptor substrate-1, phosphatidylinositol 3-kinase, and release of intracellular Ca2+ stores in
insulin stimulated
insulin secretion in beta -cells
Greenbaum et al., Diabetes 2001 (Diabetes Mellitus, Type 1...) :
Of the 585 OGTTs performed on islet cell antibody ( ICA ) -positive relatives with
insulin autoantibodies (IAA) or low first-phase
insulin response ( FPIR ), normal glucose tolerance ( NGT ) was found in 427 subjects ; impaired glucose tolerance ( IGT ) was found in 87 subjects, and diabetes was found by 2-h OGTT criteria alone in 61 subjects
Marinchenko et al., Proc Soc Exp Biol Med 1992 :
Insulin proteolysis was
inhibited by specific
insulin protease inhibitors and stimulated by disulfide reducing agents
Ellis et al., Obesity (Silver Spring) 2010 (Obesity) :
Intravenous glucose tolerance tests were also performed to adjust for fasting insulin, acute
insulin response to glucose, and
insulin sensitivity
Golden et al., Metabolism 1985 (Diabetes Mellitus, Lipoatrophic...) :
Binding of insulin to IgG, IgM, and IgE was not increased,
insulin binding to monocytes and erythrocytes was not sufficiently abnormal to account for the the insulin resistance, and insulin receptor
increased insulin clearance or accelerated degradation of
insulin by tissues
Liu et al., J Biol Chem 2007 (Insulin Resistance) :
Knocking down the PTEN gene prevented oleate to inhibit
insulin activation of Akt and
insulin suppression of gluconeogenesis
Smith et al., J Appl Physiol 2004 (Insulin Resistance) :
Insulin stimulated tyrosine phosphorylation of
insulin receptor substrate (IRS)-1 was reduced by levodopa-carbidopa, although Akt phosphorylation was unaffected by levodopa-carbidopa
Rabinovitch et al., Endocrinology 1988 :
After an 18-h preincubation in medium with 0.1 and 1 U/ml IL-1,
insulin release responses to 16.7 mM glucose were abolished in 4-h incubations, whereas responses to 0.1 mM 3-isobutyl-1-methylxanthine were normal, and after a further 2 and 5 days of incubation in IL-1-free medium,
insulin responses to 16.7 mM glucose
recovered fully
Henningsson et al., Am J Physiol Cell Physiol 2001 (Endotoxemia) :
Basal plasma glucagon, islet cAMP and cGMP content after in vitro incubation, the
insulin response to glucose in vivo and in vitro, and the
insulin and glucagon
responses to the adenylate cyclase activator forskolin were greatly increased after LPS
Loh et al., Diabetologia 2012 (Diabetes Mellitus, Type 2...) :
Blood glucose and
insulin levels, insulin and glucose tolerance, and
insulin induced muscle insulin receptor
activation and downstream PI3K/Akt signalling remained unaltered in chow fed Mck-Cre ; Ptpn2 ( lox/lox ) versus Ptpn2 ( lox/lox ) mice
Dominici et al., J Endocrinol 2002 (Growth Disorders) :
Insulin stimulated phosphorylation of
insulin receptor substrate (IRS)-1 and IRS-2 was increased by 61 and 72 % respectively, while IRS-1 and IRS-2 protein levels were increased by 76 and 95 %
Boden et al., Endocrinology 1982 :
These data suggest that in intact dogs, stimulation of beta-adrenergic receptors
enhances the release of SS,
insulin , and glucagon, while stimulation of alpha-adrenergic receptors inhibits the release of SS and
insulin without having a definitive effect on glucagon
Misbin et al., Endocrinology 1983 :
Insulin , IGF 1 and IGF 2
inhibited 125I-insulin degradation by this enzyme
Elder et al., J Clin Endocrinol Metab 2006 (Diabetes Complications...) :
We measured insulin and glucagon levels,
insulin sensitivity, acute
insulin responses to iv glucose, and the ratio of proinsulin to immunoreactive insulin
Henkel et al., Metabolism 2005 (Diabetes Mellitus, Type 2...) :
In T2DM, 2-hour
insulin response ,
insulin resistance, and early glucagon increment were significant determinants of the AUC of PG ( R=0.867 )
Hyakukoku et al., Hypertens Res 2003 (Insulin Resistance...) :
Insulin induced tyrosine phosphorylation of
insulin receptor beta subunit (IRbeta) and insulin receptor substrate-1 (IRS-1) and tyrosine/threonine phosphorylation of p44/42 MAPK ( ERK-1/2 ) were evaluated
Soliman et al., Pediatr Res 1986 (Kwashiorkor...) :
Serum
insulin-like growth factors I and II concentrations and growth hormone and
insulin responses to arginine infusion in children with protein-energy malnutrition before and after nutritional rehabilitation
Højlund et al., Diabetes Obes Metab 2006 (Insulin Resistance) :
In male twins with a high similarity in genetic and environmental background, the Trp64Arg polymorphism of the beta3AR gene is associated with lower fat mass, fasting
insulin levels and an appropriate
insulin response to glucose
Shimizu et al., J Biol Chem 1986 (Liver Neoplasms, Experimental) :
The rat hepatoma HTC cells used as a control showed very low
insulin binding, no
stimulation of TAT and DNA synthesis by
insulin , and no detectable insulin-enhancement of beta-subunit phosphorylation
Xu et al., Biochem J 1996 (Insulinoma...) :
In CHO-T cells, the net rate of fluid-phase pinocytosis was rapidly
increased 3-4-fold over the basal rate by 100 nM
insulin , with half-maximal stimulation at 2 nM
insulin , as assayed by cellular uptake of horseradish peroxidase from the medium
Kasuya et al., Biochemistry 1993 :
125I-Insulin binding to these receptors was similarly
inhibited by IGF-I and
insulin with IC50 of approximately 3 nM
van Poppel et al., J Clin Endocrinol Metab 2013 (Diabetes, Gestational...) :
In regression models, the relationship between time spent in MVPA at week 15 and changes in MVPA from 15 weeks to 24 or 32 weeks with fasting glucose, glycosylated hemoglobin, fasting insulin,
insulin sensitivity, and
insulin response at week 24 or 32 was assessed
Chen et al., Fertil Steril 2009 (Hyperandrogenism...) :
To characterize and compare the effect of DHEA and insulin plus hCG on ovarian morphology, estrous cycle, hormonal levels,
insulin sensitivity, and the
regulation of
insulin signaling in rats
Nomura et al., Biol Pharm Bull 2008 :
Luteolin significantly inhibits
insulin stimulated phosphorylation of
insulin receptor-beta subunit (IR-beta) , and apigenin, kaempferol, quercetin and fisetin, also tended to inhibit the IR-beta phosphorylation
Nistrup Madsen et al., Clin Endocrinol (Oxf) 1981 :
The influence of somatostatin ( a bolus injection of 250 micrograms i.v. followed by 6 micrograms/min for 40 min ) on the plasma cyclic AMP,
insulin , glucose and non esterified fatty acid ( NEFA )
responses to i.v. adrenaline ( 0.07 micrograms/kg body-weight/min for 20 min ) and the plasma cyclic AMP,
insulin and glucose responses to a bolus injection of i.v. glucagon ( 0.01 mg/kg BW ) were studied in normal subjects
Srinivas et al., Mol Endocrinol 1993 :
The
insulin dependent tyrosine kinase activity ( TKA ) of the
insulin receptor (IR) plays an essential role in insulin signaling
Berniakovich et al., J Biol Chem 2008 (Obesity) :
We report that
insulin activates the redox enzyme activity of p66 ( Shc ) specifically in adipocytes and that p66 ( Shc ) -generated ROS
regulate insulin signaling through multiple mechanisms, including AKT phosphorylation, Foxo localization, and regulation of selected insulin target genes
Pi-Sunyer et al., J Clin Endocrinol Metab 1999 (Obesity) :
There are experimental data showing a definite
role for
insulin and glucocorticoids in the regulation of leptin, and of leptin in the regulation of
insulin
Vaarala , Ann N Y Acad Sci 2002 (Diabetes Mellitus, Type 1...) :
This suggests that
insulin-specific immune response
induced by dietary
insulin may not be controlled in children prone to beta cell autoimmunity
Schnuerer et al., Regul Pept 1987 :
GRP inhibited glucose stimulated
insulin responses, and the
insulin responses to glucose plus GIP ; unlike galanin, GRP inhibited both glucose- and GIP stimulated insulin release
Andersen et al., Acta paediatrica Scandinavica 1988 (Cystic Fibrosis) :
The total
insulin secretion during oral glucose tolerance test as judged by the area beneath the insulin curve was similar in the two groups, but
insulin secretion was significantly
delayed in patients with CF. Insulin receptor binding to monocytes and the number of receptors were significantly increased ( p less than 0.01 and 0.02, respectively ) in patients with CF whereas the dissociation constant was similar in patients with CF and controls
Eizirik et al., Pharmacol Toxicol 1987 :
The BCAA islets furthermore maintained a slightly higher insulin release to the culture medium,
insulin content and
insulin response to an acute glucose stimulus
Bevilacqua et al., Metabolism 1985 (Diabetes Mellitus, Experimental...) :
Insulin mediated glucose uptake ( insulin clamp ), endogenous glucose production, and glucose stimulated
insulin secretion ( hyperglycemic clamp ) were measured in awake dogs before and four to six weeks after streptozotocin induced diabetes mellitus
Garcia-Lorda et al., Eur J Endocrinol 2003 :
LIPID decreased leptin in the face of this
insulin induced increase (
LIPID+INS ), between 360 min ( P=0.017 ) and 420 min ( P=0.003 ), with a 23 % suppressive effect at 420 min. LIPID+DEX elevated leptin levels by 112.5+/-35.8 % at 480 min ( P=0.037 ), however, the Intralipid/heparin infusion did not blunt the rise of leptin under these conditions
Shah et al., Endocrinology 1995 (Liver Neoplasms, Experimental) :
The results of this and previous studies suggest that 1 ) the translocation of insulin to the cytoplasm, 2 ) the regulation of insulin degradation in the cytoplasm by IDE, 3 ) the possible interaction of insulin with cytoplasmic proteins other than IDE, and 4 ) the subsequent accumulation of intact insulin or
insulin complexed with cytoplasmic proteins in nuclei may
play a role in
insulin 's regulation of gene transcription and cell proliferation
Taborsky et al., Diabetes 1980 :
Previous studies have demonstrated that exogenous
insulin , injected into central cerebrospinal fluid cavities of dogs,
stimulates the release of endogenous
insulin from the pancreas
Ito et al., Keio J Med 1998 (Insulin Resistance) :
We were able to predict the degree of the plasma glucose response occurring after an impulse-like increase in plasma
insulin at 1 mU/mL, as well as the plasma
insulin response triggered by an impulse-like increase in plasma glucose at 1 mg/dL, in the form of `` impulse response curves ''
Hirose et al., Br J Pharmacol 2002 :
Immunoprecipitation and immunoblotting were used to detect
insulin mediated tyrosine phosphorylation of both IR-beta and
insulin receptor substrate (IRS)-1 , and insulin stimulated binding of IRS-1 to p85 regulatory subunit of phosphatidylinositol 3-kinase (PI3-K) in the extracted muscle
Dominici et al., J Endocrinol 2000 :
ects is associated with : ( 1 ) increased IR abundance, ( 2 ) increased
insulin stimulated IR tyrosine phosphorylation, ( 3 ) normal efficiency of IRS-1 and Shc tyrosine phosphorylation and ( 4 ) normal activation of PI 3-kinase by
insulin
Johnson et al., J Clin Endocrinol Metab 2001 :
The children returned for 3-6 annual visits for measurement of fasting insulin,
insulin sensitivity ( Si ), and acute
insulin response ( AIR ) from the tolbutamide modified frequent sampling iv glucose tolerance test and for determination of body composition by dual energy x-ray absorptiometry
Hermans et al., Diabetes 1999 (Diabetes Mellitus, Type 2...) :
Beta-cell function assessed from HOMA and beta-cell function assessed from CIGMA ( CIGMA % beta ) ( using immunoreactive insulin ) had higher DRs than first-phase intravenous glucose tolerance test derived incremental insulin peak, area,
insulin-to-glucose index, and acute
insulin response to glucose from FSIVGTT-MinMod
Isami et al., Diabetologia 1996 :
Bradykinin also enhanced
insulin stimulated GLUT4 translocation from the intracellular fraction to the cell membrane, and
insulin induced phosphorylation of the insulin receptor beta subunit and insulin receptor substrate-1 (IRS-1) without affecting the binding affinities or numbers of cell surface insulin receptors in dog adipocytes
Kashiwagi et al., J Clin Invest 1983 (Diabetes Mellitus...) :
To assess possible cellular mechanisms of in vitro resistance in noninsulin dependent diabetes mellitus ( NIDDM ), maximum
insulin stimulated glucose transport and utilization and
insulin binding were measured in adipocytes isolated from weight matched normal glycemic subjects and patients with NIDDM
Dransfeld et al., Biochem J 2001 :
This was paralleled by a slight reduction in the
insulin induced tyrosine phosphorylation of
insulin receptor substrate (IRS)-1 and IRS-2
van Dijk et al., J Endocrinol 1988 :
Rat
insulin-like growth factor (IGF)-II in the
presence of
insulin promoted a dose dependent increase in mitogenic activity, with a half-maximal concentration of approximately 1 microgram/l ; IGF-II had no effect in the absence of insulin
Knutson , J Biol Chem 1991 :
The insulin receptor beta subunit is lost from the cellular membranes of insulin treated 3T3-C2 fibroblasts with a time course superimposable with the
insulin induced loss of cellular
insulin binding activity
Naruse et al., Diabetes 2006 (Atherosclerosis...) :
Thus, activation of PKCbeta in endothelial cells and vascular tissue inhibits Akt activation by
insulin and VEGF,
inhibits Akt dependent eNOS regulation by
insulin , and causes endothelial dysfunction in obesity associated insulin resistance
Nasrin et al., Proc Natl Acad Sci U S A 1990 (Carcinoma, Hepatocellular...) :
Two independent cis acting
insulin response elements (IREs) in the gene encoding glyceraldehyde-3-phosphate dehydrogenase [ D-glyceraldehyde-3-phosphate : NAD+ oxidoreductase ( phosphorylating ), EC 1.2.1.12 ], designated IRE-A and IRE-B, are
sufficient to direct
insulin-inducible gene expression
Keeton et al., Endocrinology 2005 (Carcinoma, Hepatocellular...) :
In the present work,
insulin 's
regulation of expression of activating transcription factor 3 ( ATF-3 ), the putative transcription factor proline-rich induced protein (Pip)92, and
insulin-inducible gene-1 (Insig-1) ( an ER resident protein involved in regulation of sterol-responsive element binding protein 1 activation ) have been examined in a liver derived cell line ( rat H4IIE hepatoma cells )
Liu et al., J Neurosci Methods 2012 :
Insulin ( 0.5 and 1 U/kg )
led to a significant increase of
insulin in both plasma and CSF at 2 h after intraperitoneal administration and decreased blood glucose for at least 2h
Frittitta et al., J Cell Biochem 1995 (Cell Transformation, Neoplastic) :
In two cell lines transfected with and overexpressing human insulin receptors (IR) ( 223.8 and 184.5 ng IR/10 ( 6 ) cells ), but not in untransfected cells,
insulin binding and tyrosine kinase activity were elevated, and
insulin induced a dose dependent increase in colony formation in soft agar
Oliveira et al., Am J Physiol Endocrinol Metab 2004 :
Cold exposure promoted significantly lower
insulin induced tyrosine phosphorylation of the
insulin receptor (IR) and Ser473 phosphorylation of acute transforming retrovirus thymoma ( Akt ) and an insulin independent increase of Thr172 phosphorylation of adenosine 5'-monophosphate activated protein kinase ( AMPK )
Bikman et al., Am J Physiol Regul Integr Comp Physiol 2010 (Insulin Resistance...) :
With a longer incubation, we observed that myotubes from morbidly obese individuals appear to be largely resistant to the detrimental effects of 16 h lipid exposure as was evident, in contrast to the lean, by the absence of a reduction in
insulin stimulated
insulin receptor substrate (IRS)-1 Tyr phosphorylation, phospho-Akt, and phospho-AS160 ( P < 0.05 )
Chiu et al., Diabetes Care 2000 :
Insulin sensitivity index and the second-phase
insulin response differed among the 4 groups ( P = 0.0023 and P = 0.0082, respectively ), whereas the first-phase insulin response was marginally different ( P = 0.1090 )
Ke et al., J Biol Chem 2007 :
Moreover, increased expression of Doc2beta
enhanced glucose stimulated
insulin secretion by approximately 40 %, whereas siRNA mediated depletion of Doc2beta attenuated
insulin release
Kerr et al., Biochem Pharmacol 2010 :
At 14 days, Lira-gammaGlu and Liraglutide markedly improved glucose tolerance ( 1.4-3.4-fold ; p < 0.05 to p < 0.001 ),
insulin response to glucose ( 1.4-1.5-fold ; p < 0.05 ), insulin sensitivity ( 1.3-1.4-fold ; p < 0.05 to p < 0.01 ), as well as increasing pancreatic
insulin content ( 1.4-fold ; p < 0.05 )
Montefusco et al., Acta Diabetol Lat 1983 :
This indicates that the effect of glucose on the central dopaminergic system is mediated by pancreatic
insulin , even in the
presence of endogenous brain
insulin
Chang et al., J Clin Endocrinol Metab 2006 (Insulin Resistance) :
Insulin sensitivity ( S ( I ) ), acute
insulin response to iv glucose ( AIRg ), and disposition index ( AIRg x S ( I ), or beta-cell compensation for insulin resistance ) from frequently sampled iv glucose tolerance testing, and ISR area under the curve ( or beta-cell sensitivity to glucose ) from ramp clamp were determined
Xi et al., Hepatology 2011 (Insulin Resistance) :
Liver tissues derived from hCRP treated rats showed reduced
insulin stimulated
insulin receptor substrate (IRS) tyrosine phosphorylation, IRS/phosphatidylinositol 3-kinase (PI3K) association, and Akt phosphorylation, consistent with hCRP induced impairment of hepatic insulin signaling
Del Aguila et al., Am J Physiol Endocrinol Metab 2000 (Pain) :
Insulin stimulated
insulin receptor substrate (IRS)-1 tyrosine phosphorylation was 45 % lower after ECC ( P < 0.05 )
Sánchez-Gurmaches et al., J Exp Biol 2012 :
Insulin , growth hormone and TNFa all diminished expression of adipoR2 in adipocytes and adipoR1 in myotubes, while
insulin increased the expression of adipoR2 in the muscle cells
Boyd et al., Am J Physiol 1983 :
We have examined the
effect of
insulin and tunicamycin, which cause decreases in cell surface insulin receptor numbers in peripheral tissues, on
insulin receptors in neuron enriched brain cell cultures
Garnett et al., Clin Endocrinol (Oxf) 2010 (Diabetes Mellitus, Type 2...) :
Young people with normal fasting glucose and fasting insulin < or =180 pmol/l had lower insulin resistance ( homeostasis model assessment median 1.9 vs. 4.2, P < 0.001 ), higher
insulin sensitivity index ( 2.4 vs. 1.0, P < 0.001 ) and a lower early
insulin response ( insulinogenic index 2.5 vs. 4.1, P < 0.001 ) compared to those with normal fasting glucose and higher fasting insulin levels
Wang et al., Biochem J 1998 :
The hormone also caused a marked reorganization of actin filaments, which was prevented by cytochalasin D. Cytochalasin D also decreased significantly the
insulin dependent association of PI 3-kinase activity and the levels of
insulin receptor substrate (IRS)-1 , p85alpha and p110beta with immunopurified GLUT4 containing compartments
Lee et al., Am J Physiol Heart Circ Physiol 2010 (Disease Models, Animal...) :
These findings were explained by increased myocardial content of p85alpha ( regulatory subunit of PI 3-kinase ), diminished association of PI 3-kinase with
insulin receptor substrate (IRS)-1 in
response to
insulin , and increased serine-307 phosphorylation of IRS-1
Neely et al., J Invest Dermatol 1991 (Carcinoma, Squamous Cell...) :
Insulin action was partially blocked by alpha IR-3, suggesting that
insulin can
act through both the
insulin and type I IGF receptors
Levy et al., Endocrinology 1986 (Osteosarcoma) :
In conclusion, ROS cells bind
insulin to specific receptors that are similar to insulin receptors on other target tissues ; receptors internalize insulin, which is then processed through a chloroquine-sensitive pathway ;
insulin does not
affect membrane substrate transport ; and insulin does inhibit the activity of an enzyme that is important in bone metabolism
Wu et al., Yao Xue Xue Bao 2005 :
The
insulin-liposomes coated by chitosan and its derivatives can enhance enteral absorption of insulin and
increase stability of
insulin in GI tract
Takayama et al., Proc Natl Acad Sci U S A 1984 (Liver Neoplasms, Experimental) :
PMA ( 0.1-1.0 micrograms/ml ) did not affect
insulin binding either acutely or chronically but
inhibited insulin stimulation of glycogen synthase and tyrosine aminotransferase
Gupta et al., Neurochem Int 1992 (Diabetes Mellitus, Experimental) :
Insulin receptors from rat brain regions were studied for insulin binding and receptor associated kinase activity, in alloxan induced short-term and long-term diabetes, and
insulin induced hypoglycemia
Bray , Proc Nutr Soc 2000 :
The dip in glucose is preceded by a rise in
insulin , and
stimulating insulin release will decrease circulating glucose and lead to food intake
Yamauchi et al., Mol Cell Biol 1994 :
Transient transfection of parental CHO cells with an insulin receptor substrate 1 (IRS1) expression plasmid
enhanced insulin downstream signaling in a biphasic manner, whereas IRS1 transfection of CHO/IR cells inhibited
insulin signaling in a dose dependent fashion
Westerlund et al., Diabetes 2002 :
An insulin-mimetic compound ( L-783,281 ) was used in an attempt to determine the
role of the beta-cell
insulin receptor (IR) on
insulin release
Zhu et al., Mol Endocrinol 2013 :
One potential mechanism is PI3K- and Akt mediated activation of mechanistic target of rapamycin (mTOR) and ribosomal protein S6 kinase (S6K), which may impair
insulin mediated activation of
insulin receptor substrate (IRS)1/2 via inhibitory serine phosphorylation or proteasomal degradation
Gasparro et al., Biochem Biophys Res Commun 1986 :
The UVA induced activity of
AMT-insulin can be
blocked by the presence of native
insulin
Yuan et al., PloS one 2011 (Body Weight...) :
Glucose tolerance test and
insulin tolerance test (ITT) in vivo and glucose
stimulated insulin secretion ( GSIS ) test in vitro were performed at different stages in IUGR and normal groups
Wang et al., Biochem Biophys Res Commun 2006 (Insulin Resistance) :
The results showed that
insulin induced tyrosine phosphorylation of
insulin receptor substrate (IRS)-2 was significantly blocked
Sprynski et al., Leukemia 2010 (Multiple Myeloma) :
Insulin is an MGF as potent as IGF-1 at physiological concentrations and
requires the presence of
insulin/IGF-1 hybrid receptors, stimulating INSR ( + ) IGF-1R ( + ) MMCs, unlike INSR ( + ) IGF-1R ( - ) or INSR ( - ) IGF-1R ( - ) MMCs. Immunoprecipitation experiments indicate that INSR is linked with IGF-1R in MMCs and that insulin induces both IGF-1R and INSR phosphorylations and vice versa
Graves et al., J Biol Chem 1986 :
Phosphorylation of calmodulin was only observed in the
presence of
insulin and was both Ca2+- and
insulin concentration dependent with half-maximal effects observed at 0.1 microM free Ca2+ and 350 microunits/ml insulin
Nogueira et al., PLoS Genet 2013 (Diabetes Mellitus, Type 1...) :
GLIS3 knockdown ( KD ) in INS-1E cells, primary FACS purified rat beta cells, and human islet cells decreased expression of MafA,
Ins2 , and Glut2 and
inhibited glucose oxidation and
insulin secretion, confirming the role of this transcription factor for the beta cell differentiated phenotype
Raissouni et al., International journal of pediatric endocrinology 2012 :
Subjects underwent anthropometric measurements, steroid profiling and frequently sampled Intravenous Glucose Tolerance Test ( IVGTT ), Homeostasis Model Assessment ( HOMA ) index, Glucose Disposal Index ( GDI ), Acute
Insulin Response ( AIR ) and Quantitative
insulin sensitivity check index ( QUICKI ) were derived from IVGTT results
Wolfsheimer et al., Am J Vet Res 1986 :
Intravenous glucose tolerance tests ( 600 mg/kg ) were administered before and after treatment to evaluate plasma glucose in fasting dogs, glucose fractional clearance rate, serum insulin in fasting dogs,
insulin peak
response , total
insulin secretion, and insulinogenic index
Cerveny et al., Ann Pharmacother 1998 (Diabetes Mellitus, Type 2...) :
People with type 1 diabetes have an absolute deficiency of insulin, whereas people with type 2 diabetes have varying degrees of
insulin resistance and an inadequate compensatory
insulin secretory
response
Demkow et al., J Physiol Pharmacol 2008 :
Isolated granulocytes were
stimulated by fMLP or
insulin alone, or by both substances added to the medium in combinations : fMLP + insulin ( after 20 min ) or
insulin + fMLP ( after 20 min )
Weinstock et al., Am J Physiol 1993 (Liver Neoplasms, Experimental) :
Insulin stimulated beta-actin transcription 11.4-fold and gamma-actin 8.4-fold at 30 min. alpha-Tubulin transcription was
induced by both
insulin and calcium ionophores but to a lesser degree
Berggreen et al., Am J Physiol Endocrinol Metab 2009 :
Pretreatment of primary rat and 3T3L1 adipocytes with Akti resulted in dose dependent inhibition of PKB phosphorylation and activation in response to insulin, without affecting upstream
insulin signaling [ insulin receptor (IR), insulin receptor substrate (IRS) ] or the
insulin induced phosphoinositide 3-kinase (PI3K) dependent
activation of the ERK/p90 ribosomal kinase ( RSK ) pathway
Leibiger et al., FEBS Lett 2002 :
While, historically, insulin was suggested to exert a negative effect on beta-cells, recent data provide evidence for a positive
role of
insulin in transcription, translation, ion flux,
insulin secretion and beta-cell survival
Miura et al., Biochim Biophys Acta 1999 (Insulin Resistance) :
10 nM
insulin stimulated activation of tyrosine kinase, IRS-1 and PI3K was suppressed by preincubation with 0.1-10 nM TNF-alpha for 60 min. 10 nM TNF-alpha pretreatment also
suppressed 10 nM
insulin- and 1 microM TPA induced increases in membrane associated PKCbeta and PKCzeta
Ueki et al., Mol Cell Biol 2004 (Endotoxemia...) :
In concordance with these increases by LPS, tyrosine phosphorylation of the
insulin receptor (IR) is partially impaired and phosphorylation of the
insulin receptor substrate (IRS) proteins is almost completely
suppressed
Usui et al., EMBO J 2004 :
In this study, we demonstrate that microinjection of anti-GRK2 antibody or siRNA against GRK2 increased
insulin stimulated
insulin-responsive glucose transporter 4 (GLUT4) translocation, while adenovirus mediated overexpression of wild-type or kinase-deficient GRK2 inhibited insulin stimulated GLUT4 translocation as well as 2-deoxyglucose uptake
Sekine et al., J Nutr Sci Vitaminol (Tokyo) 2013 :
Dietary MCT promotes
insulin secretion from the pancreas, and
insulin activates mammalian target of rapamycin (mTOR) complex 1 ( mTORC1 ) via the activation of phosphoinositide 3-kinase (PI3K) and its downstream effecter, Akt
Axen et al., Am J Physiol 1982 :
In isolated, perfused ethionine treated pancreases secretin failed to stimulate insulin secretion, whereas basal
insulin secretion and
insulin responses to glucose, arginine, gastric inhibitory polypeptide, vasoactive intestinal peptide (VIP), and somatostatin were similar to those of controls
Hrytsenko et al., Gen Comp Endocrinol 2008 :
Since the basal level of insulin mRNA was approximately 3.7-fold higher in tilapia beta-cells than it is in mammalian beta-cells,
insulin production in tilapia cells probably relies on an enlarged intracellular insulin mRNA pool and does not
require the transcriptional activation of the
insulin gene
Hans et al., Bioorg Med Chem 2010 :
These results and modeling of INS-2, C-INS-2 and C-INS-2-OH into the 3D structure of PDHP and PP2Calpha, suggest that
INS-2 binds to distinctive sites on the two different phosphatases to
activate insulin signaling
Goren et al., Cell Signal 1990 :
pp180 was a substrate for the
insulin receptor : ( i ) receptor and pp180 phosphorylation followed a similar insulin dose-response, although fold-stimulation of autophosphorylation was greater ; and ( ii ) removal of
insulin receptors with monoclonal antibodies
prevented subsequent pp180 phosphorylation
Krarup et al., Diabete Metab 1984 (Diabetes Mellitus, Type 1) :
The
effect of
insulin on the secretion of immunoreactive gastric inhibitory polypeptide,
insulin ( as measured by C-peptide ), glucagon and pancreatic polypeptide during and after a test meal was examined in seven diabetic patients treated with high insulin doses ( mean 1.12 +/- 0.12 IU/kg X 24 h ) before and after a reduction of the insulin dose ( to 0.62 +/- 0.04 IU/kg X 24 h, p less than 0.02 )
Aquila et al., Endocrinology 2005 :
The simultaneous decrease in both
insulin release and glucose-6-phosphate dehydrogenase activity
induced by blocking the autocrine
insulin effect with three different procedures ( blockage of insulin release by nifedipine, immune neutralization of the released insulin by antiinsulin serum, and blockage of an insulin intracellular effector such as phosphotidylinositol 3-kinase by wortmannin ) strongly suggests a physiological role of sperm insulin on these two events
Ventura et al., Arch Pediatr Adolesc Med 2009 (Diabetes Mellitus, Type 2...) :
Body composition by dual-energy x-ray absorptiometry ; visceral adipose tissue by magnetic resonance imaging ; glucose and insulin incremental area under the curve by oral glucose tolerance test ;
insulin sensitivity, acute
insulin response , and disposition index by intravenous glucose tolerance test ; and dietary intake by 3-day records
Srivastava et al., Diabetes 2003 :
To determine whether constitutively secreted
insulin is
necessary for glucose stimulated
insulin secretion, CD1 male mouse islets were incubated for 30 min at 4 degrees C in the absence ( control ) or presence of anti-insulin ( 1 micro g/ml ) or anti-IgG ( 1 micro g/ml )
Lillioja et al., N Engl J Med 1993 (Diabetes Mellitus, Type 2...) :
Obesity, insulin resistance ( independent of obesity ), and low acute plasma insulin response to intravenous glucose ( with the degree of obesity and insulin resistance taken into account ) were predictors of NIDDM : The six-year cumulative incidence of NIDDM was 39 percent in persons with values below the median for both
insulin action and acute
insulin response , 27 percent in those with values below the median for insulin action but above that for acute insulin response, 13 percent in those with values above the median for insulin action and below that for acute insulin response, and 0 in those with values originally above the median for both characteristics
Turk et al., Diabetes 1993 (Diabetes Mellitus, Type 2...) :
This study offers the following viewpoints on potential roles of these lipid messengers in insulin secretion as working hypotheses : 1 ) the Ca2+ signal provided to the beta-cell by D-glucose
induces insulin secretion only in the context of amplifying background signals provided by the beta-cell content of messengers including DAG ; 2 ) muscarinic receptor agonists amplify glucose induced
insulin secretion in part by altering the beta-cell content of DAG ; 3 ) the Ca2+ signal provided by metabolism of D-glucose is amplified by the level of nonesterified arachidonic acid in beta-cell membranes, which acts to facilitate Ca2+ entry ; 4 ) metabolism of glucose induces accumulation of nonesterified arachidonate in beta-cells via activation of a recently identified ASCI-PLA2 enzyme, which may be a component of the beta-cell fuel sensor apparatus ; and 5 ) arachidonate 12-LO metabolites are potential candidates as adjunctive modulators of beta-cell K ( + ) -channel activity
Castaño et al., Diabetes 1993 (Diabetes Mellitus, Type 1) :
Guinea pig, fish
insulin , and insulin containing Trp rather than Leu in position 13 of the A-chain
inhibited minimally the human
insulin binding
Björntorp , Diabetes Metab Res Rev 1999 (Insulin Resistance) :
Cortisol counteracts the insulin activation of glycogen synthase in muscle, the
insulin inhibition of hepatic glucose production and the
insulin inhibition of lipolysis in adipose tissue, leading to the well established systemic insulin resistance caused by excess cortisol
Bonadonna et al., Metabolism 1990 (Insulin Resistance...) :
Insulin mediated glucose metabolism ( euglycemic insulin clamp at plasma insulin concentration of 100 microU/mL ) and glucose stimulated
insulin secretion ( hyperglycemic clamp ) were examined in 42 obese subjects ( ideal body weight [ IBW ], 158 +/- 4 % ) with normal glucose tolerance and in 36 normal weight ( IBW, 102 % +/- 1 % ) age matched controls
Laws et al., Arterioscler Thromb 1994 (Hyperlipidemias...) :
Resistance to
insulin stimulated glucose uptake and to
insulin suppression of free fatty acid levels in Asian Indians is associated with a number of metabolic abnormalities that are demonstrated risk factors for coronary heart disease, including increased glucose, insulin, and triglyceride concentrations and decreased high-density lipoprotein cholesterol concentrations
Hribal et al., FASEB J 2003 :
Recent evidence suggests that
insulin signaling through the insulin receptor A type ( Ex11- ),
regulates insulin gene transcription
Wu et al., Biochem J 1999 :
Insulin stimulates pancreatic-duodenal homoeobox factor-1 ( PDX1 ) DNA binding activity and
insulin promoter activity in pancreatic beta cells
Shibata et al., J Biol Chem 2010 :
Under these conditions, oxidative stress did not affect
insulin dependent tyrosine phosphorylation of insulin receptor,
insulin receptor substrate (IRS)-1 and -2, or binding of the phosphatidylinositol 3'-OH kinase ( PI 3-kinase ) p85 regulatory subunit or p110alpha catalytic subunit to each IRS
Wilmore et al., Ann Surg 1976 (Body Weight...) :
Fasting serum insulin concentrations were comparable in the 12 normals and 17 hypermetabolic burn patients ( 22 +/- 3muU/ml in normals vs 22 +/- 2 ), as was fasting insulin corrected for fasting glucose ( 24 +/- 3 in normals vs 21 +/- 3, NS ), initial
insulin response ( 0-10 min delta insulin, 58 +/- 13 in normals vs 67 +/- 10, NS ) or total
insulin response corrected per unit glycemic stimulus ( insulinogenic index, 0.48 +/- 0.10 in normals vs 0.52 +/- 0.07, NS )
Lindsay et al., J Clin Endocrinol Metab 2004 (Birth Weight...) :
It is proposed that
insulin antibodies (IA) allow transfer of
insulin across the placenta, contributing to fetal hyperinsulinemia and macrosomia
Iafusco , Acta Biomed Ateneo Parmense 2005 (Diabetes Mellitus, Type 1) :
Since children with diabetes are, often, totally c-peptide negative, insulin therapy must substitute the absence of
insulin production and the successful use of short acting insulin analogues
requires optimal association with basal
insulin
Petersen et al., Am J Med 2006 (Diabetes Mellitus, Type 2...) :
This defect appears to be a result of intracellular lipid induced inhibition of
insulin stimulated
insulin-receptor substrate (IRS)-1 tyrosine phosphorylation resulting in reduced IRS-1 associated phosphatidyl inositol 3 kinase activity
Robert et al., Diabetes Care 1991 (Diabetes Mellitus, Type 1) :
Determinations were made of 1- and 3-min
insulin responses to glucose ( 0.5 g/kg i.v. ), islet cell antibodies ( ICAs ),
insulin autoantibodies (IAAs), and HLA
Santos et al., Diabete Metab 1995 (Diabetes Mellitus, Type 2) :
There was no change in erythrocyte insulin receptor binding associated with metformin treatment, but both basal and
insulin stimulated insulin receptor tyrosine kinase activities of solubilized erythrocyte
insulin receptors were significantly higher after 10 weeks of metformin treatment
Simonis-Bik et al., Diabetologia 2011 (Insulin Resistance) :
Insulin sensitivity, insulinogenic index,
insulin response and postprandial glycaemia were assessed, as well as model derived parameters of beta cell function, in particular beta cell glucose sensitivity and insulin secretion rates
Chen et al., Am J Physiol Heart Circ Physiol 2006 (Diabetes Mellitus, Type 2...) :
No significant changes in fasting glucose ( 156 +/- 11 mg/dl ),
insulin ( 14 +/- 2 microU/ml ), SI ( Clamp ) [ 2.71 +/- 0.46 x 10 ( -4 ) dl x kg ( -1 ) x min ( -1 ) / ( microU/ml ) ], or forearm blood flow in
response to ACh, SNP, or
insulin were observed after vitamin C treatment
Poretsky et al., J Clin Endocrinol Metab 1988 :
This possible effect of
insulin on the ovary could be
mediated by either the insulin receptor or the type I
insulin-like growth factor (IGF) receptor, both of which have been described in the human ovary
Miralles et al., Diabetes 1990 :
Infusion of rat galanin reduced unstimulated
insulin release ( approximately 60 %, P less than 0.01 ) and the
insulin responses to arginine ( approximately 30 %, P less than 0.025 ), glucose ( 100 %, P less than 0.01 ), and VIP ( approximately 80 %, P less than 0.025 )
Riccio et al., Diabetes Care 1994 (Diabetes Mellitus, Type 1...) :
Daily plasma glucose concentration averaged 10.3 +/- 0.3 mM and the area under the curve ( AUC ) was 1.41 +/- 0.05 mol/14 h. NPH
insulin , given at suppertime for a month, did not
induce significant changes in fasting plasma
insulin ( 40.2 +/- 4.8 pM ), glucose concentration ( 14.0 +/- 0.9 mM ) or HGP ( 20.2 +/- 2.2 mumol.kg-1.min-1 )
Henriksen , Am J Physiol Regul Integr Comp Physiol 2007 (Diabetes Mellitus, Type 2...) :
ANG II treatment of L6 myocytes causes impaired
insulin receptor substrate (IRS)-1 dependent
insulin signaling that is accompanied by augmentation of NADPH oxidase mediated ROS production ... The TG ( mREN2 ) 27 rat displays whole body and skeletal muscle insulin resistance that is associated with local oxidative stress and a significant reduction in the functionality of the
insulin receptor (IR)/IRS-1 dependent
insulin signaling
Ikeda et al., Metabolism 1993 :
The GIP induced ( 2 or 20 micrograms )
insulin release was partly inhibited by propranolol pretreatment ( 0.5 mg/kg subcutaneously [ SC ] ), and GLP-1 induced ( 2 or 20 micrograms )
insulin release was partly
inhibited by propranolol or metoprolol ( 35 mg/kg SC )
He et al., J Biol Chem 2003 (MAP Kinase Signaling System) :
Expression of FLNaCT had no major effect on
insulin induced phosphorylation of the IR,
insulin receptor substrate-1, or AKT, but it elicited changes in actin cytoskeletal structure and ruffle formation in HepG2 cells
Zawalich et al., J Biol Chem 2002 :
Effects of glucose, exogenous
insulin , and carbachol on C-peptide and
insulin secretion from isolated perifused rat islets
Caruso et al., Diabetes 2000 (Diabetes Mellitus, Type 2) :
Hepatocytes without the insulin receptor gene and expressing IR1152 ( Hep ( MUT ) ) also showed normal
insulin suppression of glucose production and full
insulin response of glycogen synthase
Wuesten et al., Horm Metab Res 2001 :
Glucose and insulin data were analyzed by minimal model assumptions - glucose sensitivity of the beta-cells ( Theta1 ), acute
insulin response ( AIR ) ( 10 min ), 3 h
insulin release ( Theta2 ), glucose threshold of insulin secretion ( h ), insulin degradation rate ( n ), peripheral insulin sensitivity ( S ( I ) ), and glucose dependent glucose disposal ( S ( G ) )
Inoue et al., Horm Metab Res 1993 :
Amylin did not alter glucose stimulated secretion of
insulin but significantly
inhibited arginine stimulated secretion of
insulin ( control : 20.9 +/- 1.4 pmol/min ; amylin group : 14.8 +/- 1.6 pmol/min, p < 0.05 )
Alvarez et al., Horm Metab Res 1987 :
The reduced [ 125I ] -insulin binding observed in adult hepatocytes was dependent on the concentration of insulin and on the duration of exposure, while in fetal hepatocytes
insulin did not
induce any reduction in
insulin binding
Leibiger et al., Annu Rev Nutr 2008 (Diabetes Mellitus, Type 2...) :
Although insulin historically has been suggested to exert a negative effect on beta-cells, recent data provide evidence for a positive
role of
insulin in transcription, translation, ion flux,
insulin secretion, proliferation, and beta-cell survival
Jepson et al., Br J Nutr 1988 (Body Weight) :
Insulin and free T3
stimulated each other as well as muscle protein turnover ;
insulin stimulating the RNA activity particularly at low insulin levels, free T3 stimulating the RNA content and both hormones stimulating proteolysis
Freidenberg et al., J Clin Invest 1988 (Diabetes Mellitus, Type 2...) :
Insulin stimulated kinase activity of adipocyte derived
insulin receptors is reduced in subjects with non-insulin dependent diabetes mellitus ( NIDDM ) but normal in obese nondiabetics
Frangioudakis et al., J Endocrinol 2008 (Insulin Resistance) :
Insulin stimulated
insulin receptor (IR) Tyr1162/Tyr1163 phosphorylation and IR substrate (IRS)-1 Tyr612 phosphorylation were
increased at least twofold over basal in GLYC rats with
insulin and this increase was not significantly impaired in the LIP rats
Laviola et al., Diabetes 2001 (Diabetes Mellitus, Experimental) :
The levels of
insulin stimulated tyrosine phosphorylation of the insulin receptor beta-subunit,
insulin receptor substrate (IRS)-2 , and p52 ( Shc ) were increased in diabetic compared with control heart, whereas tyrosine phosphorylation of IRS-1 was unchanged
Cruz et al., Hypertension 2002 (Insulin Resistance) :
The ethnic difference in blood pressure was not explained by body composition, fasting insulin, acute
insulin response , or
insulin sensitivity
Miele et al., J Biol Chem 2003 :
Human glycated albumin affects glucose metabolism in L6 skeletal muscle cells by impairing
insulin induced
insulin receptor substrate (IRS) signaling through a protein kinase C alpha mediated mechanism
Mayer et al., Endocrinology 2010 :
Thus, a sustained elevation of
insulin levels
diminishes neuronal
insulin signaling through mTOR-S6K1 mediated IRS-1 serine phosphorylation, proteasomal degradation of IRS-1 and lysosomal degradation of the IR
Storz et al., Eur J Biochem 1999 (Diabetes Mellitus, Type 2...) :
We here show that, although TNF downregulated
insulin induced
insulin receptor (IR) and IR substrate (IRS)-1 phosphorylation as well as phosphoinositide 3-kinase ( PI3-kinase ) activity in pmi28 myotubes, this was, unlike in adipocytes, not sufficient to affect insulin induced glucose transport
Kawabe et al., J Hypertens 2000 (Insulin Resistance) :
Assays for
insulin induced activities of
insulin receptor substrate (IRS)-1 , phosphoinositide 3-kinase (PI3-K) and mitogen activated protein kinase ( MAPK ) were performed
Li et al., Endocrinology 2005 :
Insulin at physiological concentrations selectively
activates insulin but not insulin-like growth factor I (IGF-I) or
insulin/IGF-I hybrid receptors in endothelial cells
Argentino et al., J Gerontol A Biol Sci Med Sci 2005 :
CR reduced the in vivo
insulin induced phosphorylation of the
insulin receptor substrate (IRS)-1 by 27 %, but this difference was not significant ( p =.298 )
Schwartz et al., Peptides 1990 (Hyperinsulinism...) :
In order to study the
role of plasma
insulin in regulating the binding of
insulin to the endothelium of the blood-brain barrier ( BBB ), insulin binding to a purified preparation of brain capillaries was measured in both genetically obese Zucker rats and lean Zucker controls
Stevens et al., J Biol Chem 1983 (Chondrosarcoma...) :
The
insulin induced increase in
125I-insulin binding was not associated with an increase in the binding of 125I labeled multiplication stimulating activity ( 125I-MSA ), an insulin-like growth factor
Nakai et al., Tohoku J Exp Med 1984 (Diabetes Mellitus, Experimental) :
However,
insulin-dextran complex (II)
caused a 67 % stimulation of native
insulin
Wu et al., Arch Pharm Res 2010 (Diabetes Mellitus, Type 2...) :
In this study, we used the frequently sampled intravenous glucose tolerance test ( FSIGT ) to evaluate the
insulin sensitivity (IS) , glucose sensitivity ( SG ), and acute
insulin response after glucose load ( AIRg ) after 4 months treatment with either gliclazide or repaglinide
McManus et al., Diabetes Care 1996 (Diabetes Mellitus, Type 2) :
After each 3-month period, fasting glucose and
insulin levels, HbA1c, lipid profiles, insulin sensitivity ( SI ), glucose effectiveness ( SG ), and acute
insulin response to glucose ( AIRG ) were evaluated
Yuan et al., Diabetes Res Clin Pract 2006 (Diabetes Mellitus, Type 2...) :
To measure the serum highly sensitive C-reactive protein ( hs-CRP ) and adiponectin levels, assess
insulin sensitivity index ( SI ) and acute
insulin response ( AIR ) in normal control ( NC ) subjects, patients with impaired glucose tolerance ( IGT ) and newly diagnosed type 2 diabetes mellitus ( DM ), and further explore the possible correlation between hs-CRP and SI, AIR and adiponectin in IGT and newly diagnosed type 2 DM groups
Panariello et al., J Cell Physiol 2012 (Insulin Resistance) :
Consistently, clozapine reduced
insulin effect on
insulin receptor (IR) by 40 % and on IR substrate-1 (IRS1) tyrosine phosphorylation by 60 %
Soga et al., Biochem Biophys Res Commun 2005 :
LPC potently enhances
insulin secretion in response to high concentrations of glucose in the perfused rat pancreas via stimulation of adenylate cyclase, and dose-dependently
induces intracellular cAMP accumulation and
insulin secretion in a mouse pancreatic beta-cell line, NIT-1 cells
Hosokawa et al., Diabetes 1997 (Hypoglycemia) :
Importantly, a raised
amylin-to-insulin ratio and a relatively unimpaired first versus second phase
insulin response for high glucose/arginine both occur in diabetic rats
Zhang et al., Eur J Drug Metab Pharmacokinet 2001 (Hyperlipidemias...) :
When troglitazone was administrated at a high dose for 6 months, it reduced hyperinsulinemia as reflected by a reduced basal ( steady-state )
insulin concentration lb and the
insulin response to a glucose load, improved beta-cell function as reflected by decreased second-phase post-hepatic insulin delivery to glucose phi2, and reduced insulin resistance as reflected by increased insulin sensitivity to glucose disposal Si, without affecting glucose tolerance as reflected by an unchanged rate of glucose utilization Kg or insulin independent glucose disposal Sg
Xu et al., J Biol Chem 2004 :
During 3T3-L1 preadipocyte differentiation induction, the
insulin stimulated
insulin-like growth factor-1 (IGF-1) receptor signal is responsible for the induction of adipocyte differentiation
Kalant et al., Mech Ageing Dev 1988 :
The increased
insulin responsiveness of R rats was not
due to an increase in insulin binding or to a decrease in
insulin degradation ( measured with intact cells or as cytosolic insulinase activity ). ( ABSTRACT TRUNCATED AT 400 WORDS )
Hooper et al., J Neurochem 2011 :
Following a conservative correction ( Bonferroni ) for multiple testing, seven genes were identified to be differentially expressed from controls ; four of these genes were regulated by
insulin and three genes were
regulated by both
insulin and Wnt3a
Abdo et al., Diabetologia 2013 :
In vitro,
insulin inhibited Agt but stimulated Hnrnpf and Hnrnpk expression in high-glucose media via p44/42 mitogen activated protein kinase signalling in RPTCs. Transfection with Hnrnpf or Hnrnpk small interfering RNAs
prevented insulin inhibition of Agt expression in RPTCs
Gonzalez-Rodriguez et al., Endocrinology 2007 (Insulin Resistance) :
PTP1B deficiency in immortalized neonatal hepatocytes prolonged
insulin induced tyrosine phosphorylation of the
insulin receptor (IR) and IR substrates (IRS) -1, -2 compared with wild-type control cells
Zhu et al., Invest Ophthalmol Vis Sci 2009 (Disease Models, Animal...) :
Glucagon and
insulin ( or IGF-1 )
cause generally opposite modulations of eye growth, with glucagon mostly increasing choroidal thickness and
insulin mostly increasing ocular elongation
Ward et al., Adv Exp Med Biol 1985 (Diabetes Mellitus...) :
In patients with long standing insulin dependent diabetes mellitus ( IDDM ), basal
insulin secretion and
insulin responses to all stimuli are virtually absent
Bucher et al., N Engl J Med 1983 (Body Weight...) :
We studied
insulin-like growth factors (IGF) I and II, prolactin, and the
insulin response to arginine in 19 children with craniopharyngioma and documented growth hormone deficiency
Tsao et al., Diabetes 1996 :
Plasma glucose and
insulin levels in MLC-GLUT4 mice are altered as a
result of increased
insulin action
Lioutas et al., Endocrinology 1997 :
During luteinization of bovine granulosa cells in vitro in the
presence of
insulin , or
insulin plus forskolin, there is a massive upregulation not only of progesterone production, but also of the gene for the peptide hormone oxytocin, with secretion of the peptide into the medium
de Boer et al., Kidney Int 2013 (Renal Insufficiency, Chronic) :
Paricalcitol significantly reduced serum concentrations of parathyroid hormone, 1,25-dihydroxyvitamin D, and 25-hydroxyvitamin D while significantly increasing serum concentrations of fibroblast growth factor-23 and 24,25-dihydroxyvitamin D. Paricalcitol, however, had no significant effect on glucose tolerance ( the primary outcome measure ),
insulin sensitivity, beta-cell
insulin response , plasma free fatty acid suppression, or urinary F2-isoprostane excretion
Greene et al., Biochem Biophys Res Commun 2006 :
The IRS-1 PH and PTB domains are essential for
insulin stimulated IRS-1 Tyr phosphorylation and
insulin signaling, while Ser/Thr phosphorylation of IRS-1 disrupts these signaling events
Isaac et al., J Biol Chem 2013 (Diabetes Mellitus...) :
Here, we demonstrate that incubation ( 2 h ) of murine islets or Min6 ß cell line with the SSRIs paroxetine, fluoxetine, or sertraline inhibited
insulin induced Tyr phosphorylation of
insulin receptor substrate (IRS)-2 protein and the activation of its downstream targets Akt and the ribosomal protein S6 kinase-1 ( S6K1 )
Beardsall et al., Endocr Dev 2007 (Hyperglycemia) :
Reduced
insulin levels may also
contribute to reduced
insulin-like growth factor 1 (IGF-1) generation, and an increased risk of retinopathy of prematurity
Protzek et al., Comp Biochem Physiol A Mol Integr Physiol 2010 :
Based on these data, we aimed to investigate various aspects related with glucose homeostasis analyzing : blood glucose and
insulin levels, intraperitoneal glucose and insulin tolerance tests ( ipGTT and ipITT ), glucose
stimulated insulin secretion ( 2.8, 5.6 or 8.3 mmol/L glucose ) in pancreas fragments, cellular distribution of beta cells, and the amount of pAkt/Akt in the pectoral muscle and liver
Lin et al., Br J Pharmacol 2011 (Body Weight...) :
In 3T3-L1 preadipocytes, T3 enhanced
insulin induced tyrosine phosphorylation of
insulin receptor substrate (IRS)-1 and activation of PI3-kinase, effects blocked by siRNA for TRa1
Osman et al., J Appl Physiol 2001 (Insulin Resistance...) :
Seven weeks of training significantly increased basal and
insulin stimulated ERK2 and RSK2 activities, as well as
insulin stimulation of MAPK kinase activity
Suryawan et al., J Nutr 2004 :
In this study, we examined the individual
roles of
insulin and amino acids in the activation of insulin signaling components leading to translation initiation, specifically, the
insulin receptor (IR) , insulin receptor substrate 1 (IRS-1), phosphatidylinositol 3-kinase ( PI 3-kinase ), protein kinase B (PKB) and ribosomal protein S6
Zhang et al., Cell Biochem Funct 2012 :
Subsequently, we show that although both
insulin and IGF-1
promote osteoblast differentiation and mineralization in vitro, IGF-1, but not
insulin , can induce osteoblast proliferation
Santiago et al., Am J Obstet Gynecol 1978 (Diabetes Mellitus...) :
In addition, the data suggest that exogenous
insulin may indirectly
suppress endogenous
insulin secretion and thus contribute to the `` insulin resistance '' of obese patients with maturity-onset diabetes
Afonso et al., Proc West Pharmacol Soc 2004 (Insulin Resistance) :
In SHR ipv L-NMMA
induced 26+/-5 %
insulin sensitivity inhibition ( 187.5+/-15.3 mg glucose/kg, n=6 ; P < 0.05 ), whereas in Wis, ipv L-NMMA induced 53.8+/-5.9 %
insulin sensitivity inhibition ( 138.2+/-14.7 mg glucose/kg, n=6, P < 0.05 ), significantly higher than in SHR ( P < 0.01 )
Klein et al., J Biol Chem 1987 :
We have studied how
insulin mediated internalization of insulin receptors and
insulin activation of the insulin receptor kinase might be inter related
Tanaka et al., Endocrinol Jpn 1980 :
In order to ascertain whether
insulin secretion is
inhibited by
insulin per se, the effect of exogenous rat insulin on basal and stimulated rat C-peptide reactivity (CPR) release was studied in the isolated perfused rat pancreas
Englisch et al., Biochem J 2000 :
Both IGF-I and
insulin induced net potassium uptake, while
insulin also attenuated the response to adrenaline
Miquet et al., J Mol Endocrinol 2011 :
Insulin induced tyrosine phosphorylation of the
insulin receptor (IR) was conserved in transgenic mice, but the phosphorylation of IR substrate 1 (IRS1), its association with the regulatory subunit of the phosphatidylinositol 3-kinase (PI3K), and the phosphorylation of AKT were decreased
McLaughlin et al., J Clin Endocrinol Metab 1999 (Insulin Resistance...) :
In summary, insulin mediated glucose disposal varied widely in nondiabetic, obese women, and there was no relationship between baseline
insulin resistance or total integrated
insulin response and weight loss
Koevary et al., Optometry (St. Louis, Mo.) 2004 :
In order to determine whether elevated levels of CSF
insulin could
lead to optic nerve
insulin accumulation, a separate cohort of animals was injected in their lumbar cistern with unlabeled insulin and their optic nerves later assessed for the presence of insulin by enzyme linked immunosorbent assay
Gual et al., Endocrinology 1998 :
Taking our data together, we conclude that : 1 )
insulin and IGF-1 lead to phosphorylation and activation of JAK-1 and JAK-2 in intact cells ; 2 ) phosphorylation of IRS-I by JAK-1 seems to occur on sites different from those phosphorylated by the insulin receptor ; 3 ) JAK-1 interacts directly with phosphorylated insulin and IGF-1 receptors ; and 4 ) the JH7-JH6 and JH1 domains of JAK-1 are
responsible for the interaction with
insulin and IGF-1 receptors
Grefhorst et al., Am J Physiol Gastrointest Liver Physiol 2005 (Acute Disease...) :
Insulin induced
insulin receptor substrate (IRS)1- and IRS2 associated PI3-kinase activity and PKB-phosphorylation were not affected on TDGA treatment
Pandini et al., Clin Cancer Res 1999 (Breast Neoplasms) :
Insulin and insulin-like growth factor-I (IGF-I) receptor overexpression in breast cancers
leads to
insulin/IGF-I hybrid receptor overexpression : evidence for a second mechanism of IGF-I signaling
Kadle et al., Exp Cell Res 1984 :
Insulin caused a time- and concentration dependent decrease in the number of cell surface
insulin receptors, with no significant change in total insulin receptors
Davidson et al., Biol Reprod 2002 :
The objectives of this study were to determine, first, if estradiol,
insulin , and/or FSH affect steroid production by equine granulosa cells ( experiment 1 ) and, second, if the components of the IGF system are produced by equine granulosa cells in culture as well as whether estradiol,
insulin , and/or FSH
affects IGF and/or IGF binding protein ( IGFBP ) production by equine granulosa cells ( experiment 2 )
Fischman et al., Endocr Pract 2008 (Cystic Fibrosis...) :
It is the result of multiple pathophysiologic mechanisms, including destruction of pancreatic islet cells, impaired hepatic
response to the antigluconeogenic effects of
insulin , and impaired
insulin sensitivity
Houghton et al., Eur Heart J 1998 (Heart Failure...) :
Patients with heart failure have a reduced sensitivity to
insulin 's
actions on glucose metabolism and a compensatory increase in endogenous plasma
insulin levels
Hsieh et al., Chin J Physiol 2007 (Body Weight...) :
During the test period, low-dose insulin infusion kept plasma insulin at basal levels in C and C ( TG ) and high-dose
insulin infusion
increased plasma
insulin levels about 6 times the baseline insulin level in C. Glucose infusion rate ( GIR ) was significantly higher in rats with high insulin infusion than those with low insulin infusion
Lei et al., Biomed Environ Sci 2007 (Glycosuria) :
Cadmium can influence the biosynthesis of
insulin , but does not
induce the release of
insulin
Zanini et al., PloS one 2011 :
PDX1 ( pancreatic duodenal homeobox gene-1 ),
insulin , C peptide and Glut-2 were
detected in HI-ILCs whereas BM-ILCs only expressed Glut-2 and
insulin
Wang et al., J Cell Biol 1996 :
These data indicate that : ( a ) Glut1 and Glut4 are targeted to distinct plasma membrane domains in skeletal muscle ; ( b ) Glut1 contributes to basal transport at the sarcolemma and the bulk of insulin stimulated transport is mediated by Glut4 localized in the transverse tubules ; ( c )
insulin increases the apparent surface area of transverse tubules in skeletal muscle ; and ( d )
insulin causes the unmasking of a COOH-terminal antigenic epitope in skeletal muscle in much the same fashion as it does in rat adipocytes
Bertuzzi et al., J Endocrinol 1998 :
Compared with control islets, experimental islets showed a higher basal release of true insulin and proinsulin-like-molecules (PLM), with no increase of true
insulin and PLM release in response to 16.7 mM glucose, and a paradoxical true
insulin release in response to 3.3 mM glucose ; the PLM/total insulin ratio
increased significantly after 16.7 mM glucose
Sahin et al., Gynecol Endocrinol 2004 (Insulin Resistance...) :
Glucose, insulin,
insulin resistance, androgen levels and glucose and
insulin responses to an oral glucose tolerance tests ( OGTT ) were assessed before and after a 4-week therapy period
Nelson et al., J Vet Intern Med 1999 (Cat Diseases...) :
Significant ( P < .05 ) increases occurred in postglucagon serum insulin concentrations,
insulin peak
response , and total
insulin secretion, compared with values obtained when clinical diabetes was diagnosed
Marfaing et al., Neurosci Lett 1990 (Hyperinsulinism) :
The present study was carried out to characterize the
effects of
insulin , using the euglycemic hyperinsulinemic clamp, on
insulin binding and glucose utilization in specific areas of rat brain, by autoradiographic methods
Prince et al., J Clin Invest 1980 :
Insulin can
induce a loss of
insulin receptors in these cells, and when fibroblasts are exposed to 100 ng/ml insulin for 6 h, approximately 60 % of the initial complement of cell surface receptors are lost
Kim et al., Proc Natl Acad Sci U S A 2001 (Insulin Resistance) :
Muscle-lipoprotein lipase mice had a 3-fold increase in muscle triglyceride content and were insulin resistant because of decreases in
insulin stimulated glucose uptake in skeletal muscle and
insulin activation of insulin receptor substrate-1 associated phosphatidylinositol 3-kinase activity
Pillion et al., J Biol Chem 1985 :
Insulin binding studies revealed a dose dependent inhibition of
125I-insulin binding with porcine insulin and approximately 4 X 10 ( -9 ) M
insulin was
required to produce 50 % inhibition of 125I-insulin binding, while desoctapeptide insulin, insulin-like growth factor I, and A chain of insulin had less effect on 125I-insulin binding
Sakai et al., Endocrinology 2003 (Carcinoma, Hepatocellular...) :
These studies were undertaken to analyze the
role of IGF-I,
insulin , and insulin/IGF-I hybrid receptors (HRs) in mediating IGF-I and
insulin signaling in cells that had been made insulin-resistant by treatment with glucosamine
Agewall et al., J Intern Med 1995 (Albuminuria...) :
Overnight urinary albumin excretion,
insulin mediated glucose disposal ( hyperinsulinaemic euglycaemic clamp ), blood glucose and plasma
insulin during oral glucose tolerance test, fibrinogen, von Willebrand factor and plasminogen activator inhibitor activity
Mäkelä et al., J Autoimmun 2006 (Diabetes Mellitus, Type 1...) :
Our data suggest that enteral virus infections can enhance immune response to
insulin ,
induced primarily by bovine
insulin in cow 's milk
Weigensberg et al., Diabetes Care 2005 (Diabetes Mellitus, Type 2...) :
Insulin sensitivity ( S ( i ) ), the acute
insulin response to glucose ( AIRg ), and the disposition index ( DI ; an index of beta-cell function ) were determined using the insulin modified intravenous glucose tolerance test and minimal modeling
Pandey et al., J Cardiovasc Pharmacol 2007 (Hypertension) :
Immunoblotting revealed that hyperglycemia and PPAR-gamma inhibition significantly ( P < 0.001 ) decreased
insulin stimulated
insulin receptor (IR)-beta , Akt, and glycogen synthase kinase (GSK)-3beta phosphorylation, whereas phosphotyrosine phosphatase (PTP)-1B expression was increased in VSMC from both strains
Fingar et al., J Biol Chem 1993 :
Rapamycin completely blocked activation of pp70-S6 kinase by insulin in 3T3-L1 adipocytes, but did not inhibit
insulin stimulated glucose transport, translocation of GLUT4 to the cell surface, or activation of pp90rsk or pp44mapk by
insulin
Ishiki et al., Endocrinology 2013 (Insulin Resistance) :
We examined the effect of astaxanthin on
insulin stimulated glucose transporter 4 (GLUT4) translocation, glucose uptake, and
insulin signaling in cultured rat L6 muscle cells using plasma membrane lawn assay, 2-deoxyglucose uptake, and Western blot analysis
Kamide et al., J Hypertens 2004 :
Neither 10 nor 100 microU/ml
insulin increased cellular angiotensin converting enzyme (ACE) activity ( 2.17 to 3.48-folds, P = 0.077, 0.125, respectively ) significantly, but 1000 microU/ml
insulin strongly
up-regulated ACE activity by 16.67-folds ( P = 0.001 ) in cultured EC
Giacca et al., Endocrinology 1997 :
Systemic
insulin levels increased by 215 +/- 16,310 +/- 26, and 184 +/- 15 pM, and estimated hepatic
insulin levels
increased by 398 +/- 20, 310 +/- 26, and 184 +/- 15 pM with portal, peripheral, and 1/2 periph, respectively
Willis et al., J Clin Endocrinol Metab 1995 (Polycystic Ovary Syndrome) :
In order to account for the effects of insulin on the polycystic ovary ( PCO ), despite peripheral insulin resistance in women with polycystic ovary syndrome ( PCOS ), it has been suggested that
insulin may
act through the type-I
insulin-like growth factor (IGF) receptor and not the insulin receptor
Kitabchi et al., Nihon Naibunpi Gakkai Zasshi 1991 (Hyperplasia...) :
Insulin sensitivity was determined by
insulin responses to a standard OGTT, hypoglycemic responses to an IV
insulin tolerance test (ITT) , red blood cell ( RBC ) insulin binding and receptor kinase activity, and phytohemagglutinin ( PHA ) -activated T-lymphocyte ( T-cell ) insulin binding and PDH insulin sensitivity
Schwartz et al., Endocrinology 1985 :
To investigate cellular aspects of the antagonism between endogenous GH and insulin in adipose tissue, we examined glucose metabolism,
insulin responses , and
insulin binding in adipocytes isolated from rats made GH deficient by treatment with antibodies to rat GH ( ArGH ), which neutralize the biological actions of GH
Albalat et al., Comp Biochem Physiol B Biochem Mol Biol 2007 :
To elucidate the specific role of insulin, increases of plasma
insulin were experimentally
induced by arginine and
insulin injections
Eizirik et al., Mol Cell Endocrinol 1995 :
The cytokine did not increase
insulin release in the presence of 1.7 mM glucose, but both in the presence of 5.6 or 16.7 mM glucose, or 10 mM leucine + 2 mM glutamine, it
induced a 60-100 % increase in
insulin release
Menrad et al., Anticancer Res 1991 (Carcinoma, Hepatocellular...) :
An increased LDL receptor expression was observed on A431 epidermoid carcinoma cells of the vulva in the presence of epidermal growth factor (EGF) or
insulin but not with platelet derived growth factor ( PDGF ), on HUV-EC primary endothelial cells in the
presence of
insulin or PDGF but not with EGF, and on MRC-5 diploid fetal lung cells only in the presence of PDGF
Voll et al., J Cereb Blood Flow Metab 1991 (Brain Ischemia...) :
Because of its potential clinical use in humans, the present study was undertaken to test the hypotheses that ( a ) survival and regional ischemic brain necrosis are improved by
insulin ; ( b )
insulin requires concomitant hypoglycemia to exert its neuroprotective effect ; ( c ) insulin is still neuroprotective with delayed administration after an episode of postischemic hypotension ; and ( d ) insulin is beneficial after normoglycemic, as well as hyperglycemic ischemia
Verspohl et al., Cell Signal 1995 :
The inhibitory effects of either insulin or IGF-I on insulin release are abolished by 10 ( -4 ) M GEN but not by daidzein indicating an involvement of tyrosine kinase in the inhibitory
effect of both
insulin and IGF-I on
insulin release
Eriksson et al., Diabetologia 1992 (Insulin Resistance...) :
Vanadate, but not
insulin , was also capable of
increasing insulin binding as well as insulin sensitivity in insulin-resistant cells ( treatment with N6-monobutyryl cAMP or amiloride and adipocytes from obese, aging rats )
Luzio et al., Horm Metab Res 2002 (Diabetes Mellitus...) :
Insulin sensitivity ( S ( I ) ), glucose effectiveness ( S ( G ) ), and acute
insulin response ( AIR ( 0-10 min ) ) were measured by means of a 3-hour insulin modified frequently sampled intravenous glucose tolerance test ( FSIVGTT ) before and after a single dose of valsartan
Cooney et al., EMBO J 2004 :
In the liver, despite lower IR autophosphorylation, enhanced
insulin induced tyrosine phosphorylation of
insulin receptor substrate (IRS)-1 and activation of protein kinase B (PKB) was observed
Richmond , Int J Tissue React 1983 :
3,3',5-Tri-iodo-thyronine, 10 ( -8 ) M, stimulated 1-3H-glucosamine incorporation 300 %, while
insulin , 10 ( -6 ) M, led to a 70 % augmentation and the combination of 10 ( -8 ) M 3,3',5-tri-iodo-thyronine and 10 ( -6 ) M
insulin resulted in a 400 % increase in 1-3-H-glucosamine incorporation
Delgado-Lista et al., Nutr Metab Cardiovasc Dis 2013 :
Glucose metabolism was assessed by static ( glucose, insulin, adiponectin, leptin and resistin plasma concentrations ) and dynamic ( disposition index,
insulin sensitivity index, HOMA-IR and acute
insulin response to glucose ) indices, performed at baseline and after 12 weeks of 4 dietary interventions ( high saturated fatty acid ( SFA ), high monounsaturated fatty acid ( MUFA ), low-fat and low-fat-high-n3 polyunsaturated fatty acid ( PUFA ) ) in 486 subjects with MetS
Morales et al., Biochem Biophys Res Commun 1992 :
It was found that
insulin induced not only a decrease in the number of
insulin receptors but a 30 % loss in basal and insulin stimulated acetate incorporation into total lipids as well as a decrease in the activities of enzymes related to the novo fatty acid synthesis pathway as malic enzyme and glucose-6-phosphate dehydrogenase
Marceau et al., Biochem Cell Biol 1992 :
In the present study, we examined the mRNA expression, level of protein synthesis, and fibrillar distribution of cytokeratins 8 and 18 and actin in hepatocytes, isolated from normal and dexamethasone injected rats and cultured as monolayers or spheroids in the
presence of
insulin , or from normal rat hepatocytes, cultured as monolayers in the presence of dexamethasone,
insulin , and dimethyl sulfoxide
Pekkala et al., J Dent Res 2002 (Dental Caries...) :
After 4 weeks, we measured areas of dentin formation, numbers and areas of dentinal caries lesions, and serum and urine glucose,
insulin , Ca, Na, K, and P. Exogenous insulin
increased serum and urine
insulin levels and decreased serum glucose level, but did not affect dentin formation or dentinal caries lesion formation or progression
Lu et al., Metabolism 2009 (Metabolic Syndrome X) :
Insulin degrading enzyme (IDE) plays a primary role in
insulin degradation and cellular insulin processing and therefore affects glucose and lipid metabolism
Muñoz et al., Biochem J 1995 :
On the contrary,
insulin led to a 50 % reduction in
insulin receptors present in T-tubules and in sarcolemma, demonstrating that insulin induced insulin receptor internalization affects T-tubules in the muscle fibre
Madsen et al., Eur J Biochem 1996 :
During recent years, studies of
insulin-gene regulation and, in particular, the tissue-specific transcriptional control of
insulin-gene activity have provided information on pancreas development in general
Brendel et al., Cell Transplant 1994 :
In vitro function of islets, assessed by insulin/DNA content,
insulin secretion into the culture media over 24 h and glucose-theophylline
stimulated insulin release in a dynamic perifusion system, was not significantly different between free floating and matrix preserved islets
Kogire et al., Pancreas 1991 :
At the same concentration, however, IAPP significantly ( p less than 0.05 ) inhibited carbachol stimulated ( 10 ( -7 ) M ) release of
insulin by 30 %, and CGRP significantly
inhibited carbachol stimulated release of
insulin by 33 % when compared with the control group
Brandhorst et al., Transplantation 1999 :
LTC at 22 degrees C was associated with a reduction of insulin content ( 85+/-9 vs. 152+/-10 microU/islet equivalents [ IEQ ], P < 0.01 ), 24
hr-insulin secretion ( 82+/-7 vs. 552+/-91 microU/ day/IEQ, P < 0.001 ), and integrated dynamic
insulin response to glucose ( 1093+/-124 vs. 3074+/-708 microU/60 min/100 IEQ, P < 0.05 ), compared with 37 degrees C LTC
Winzell et al., Metabolism 2007 (Body Weight...) :
Insulin clearance, as judged by elimination of intravenous human insulin, was not altered in HFD, suggesting that the observed changes in
insulin responses to glucose are
due to changes in
insulin secretion rather than to changes in insulin clearance
Postel-Vinay et al., Mol Cell Endocrinol 1987 :
These changes occurred at 4 and 40 min after insulin injection but were no longer detectable at 3 h. Colchicine treatment did not affect the initial changes in the distribution of
insulin receptors
induced by
insulin ; however, in rats treated with the low dose of colchicine, insulin binding to plasma membranes at 3 h was not fully restored
Welch et al., J Clin Endocrinol Metab 1990 (Diabetes Mellitus) :
Across all subjects, the level of fasting serum glucose was correlated inversely with both
insulin sensitivity ( r = -0.62 ; P less than 0.05 ) and acute
insulin responses ( r = -0.72 ; P less than 0.02 ) ; however, insulin sensitivity in diabetic subjects with little insulin secretion ( 0.6 +/- 0.2 ) was comparable to insulin sensitivity in diabetic subjects with near-normal responses ( 0.6 +/- 0.3 )
Lee et al., Metabolism 2005 (Atherosclerosis...) :
Insulin resistance index, presented as homeostasis model assessment insulin resistance, and glucose or
insulin responses to oral glucose tolerance test were similar between groups
Veldhuis et al., Endocrinology 1986 :
The mechanisms subserving this facilitative interaction included the following : 1 ) insulin 's synergism with LDL was profoundly attenuated by covalent modification of arginine residues in LDL by 1,2-cyclohexanedione treatment ; 2 )
insulin increased by 2- to 6-fold the number of specific high affinity LDL receptors on granulosa cells, with no change in apparent binding affinity ; 3 ) insulin augmented rates of [ 125I ] iodo-LDL internalization and degradation without enhancing nonspecific bulk fluid-phase pinocytosis ( assessed with [ 125I ] iodo-polyvinylpyrollidone ) ; 4 )
insulin increased by 2.5- to 3-fold granulosa cell content of free and esterified cholesterol ( measured by fluorometry ) in response to treatment with unlabeled LDL ; 5 ) insulin stimulated the intracellular accumulation of free [ 3H ] cholesterol and [ 3H ] cholesteryl ester, and amplified [ 3H ] progesterone secretion by granulosa cells exposed to [ 3H ] cholesteryl linoleate labeled LDL ; and 6 ) insulin action was specific in that it was not mimicked by desoctapeptide insulin, epidermal growth factor, fibroblast growth factor, or relaxin
Oshida et al., J Appl Physiol 1989 :
After 1 yr of jogging, steady-state plasma
insulin levels (I) decreased significantly, and the metabolic clearance rate of
insulin was
increased by 87 %, although insulin infusion rate during the clamp was constant for each individual
Flatt et al., Comp Biochem Physiol A Comp Physiol 1987 (Adenoma, Islet Cell...) :
At 3 days after transplantation, plasma glucose and
insulin responses to intraperitoneal glucose,
insulin , arginine and adrenaline were similar to control rats
Huppertz et al., Diabetologia 1996 :
The
effects of
insulin , insulin-like growth factor (IGF)-I, platelet derived growth factor ( PDGF ), interleukin (IL)-6 and interferon-gamma on 2-deoxyglucose uptake and
insulin receptor substrate (IRS)-1 phosphorylation were compared in 3T3-L1 cells at confluence and after differentiation to the adipocyte-like phenotype
Schmidely , Reprod Nutr Dev 1993 :
Insulin appears to be indirectly enhanced by estrogens through an increase in growth hormone, whereas androgens
reduce insulin levels
Virkamäki et al., Diabetes 2001 (Insulin Resistance) :
Study of insulin signaling indicated that
insulin induced tyrosine phosphorylation of the
insulin receptor (IR) was blunted in HiIMCL compared with LoIMCL ( 57 vs. 142 % above basal, P < 0.05 ), while protein expression of the IR was unaltered
Demozay et al., Diabetes 2008 :
Treatment of 3T3-L1 adipocytes with HNE at nontoxic concentrations leads to a pronounced decrease in insulin receptor substrate (IRS)-1/-2 proteins and in
insulin induced IRS and
insulin receptor beta (IR beta) tyrosine phosphorylation
Cong et al., Biochem J 2007 :
We conclude that
insulin and beta-agonists act directly at the adipocytes in opposing fashions to regulate the production of adiponectin and leptin, and that a PI3K-PDE3B-cAMP pathway
mediates the effects of
insulin to restore beta-agonist/cAMP suppressed secretion and expression of these two adipokines
Ida et al., Biochem Pharmacol 1996 :
It has been proposed that pervanadate induces
insulin-like effects mediated through autophosphorylation and
activation of
insulin receptor (IR) even in the absence of insulin by inhibiting protein tyrosine phosphatases
Spruijt-Metz et al., Obesity (Silver Spring) 2012 (Coronary Artery Disease) :
We cross-sectionally examined the relationship between CRP, leptin, BMI z-score, percent body fat ( % BF ) assessed by air plethysmography ( BodPod ), and
insulin sensitivity ( SI ) and acute
insulin response ( AIRg ) measured by intravenous glucose tolerance test in 51 Latina and African-American females ( 77 % Latina ), mean age 9.2 ( ±0.9 ) years, at either Tanner Pubertal Stage (TPS) 1 ( n = 25 ) or TPS 2 ( n = 26 )
Dietze et al., Diabetes 2002 :
Insulin induced tyrosine phosphorylation of
insulin receptor substrate (IRS)-1 was completely blocked, with unaltered expression of IRS-1
Mei et al., Obes Res 1996 :
Enterostatin increased basal plasma levels of
insulin , but significantly
inhibited the increase in plasma
insulin stimulated by glucose
Freidenberg et al., J Clin Endocrinol Metab 1983 (Hemolysis) :
Furthermore, 5 % albumin, 2.5 mM N-ethylmaleimide, or excess unlabeled
insulin ( 100 micrograms/ml ) inhibited insulin degradation ( even in the presence of hemolysis ) and
prevented the rise in
insulin binding
Gliozzo et al., J Cell Biochem 1998 (Breast Neoplasms) :
In many human breast cancers and cultured cell lines,
insulin receptor expression is elevated, and
insulin , via its own insulin receptor, can
stimulate cell growth
Yoshihara et al., Biochem Biophys Res Commun 2012 :
Insulin receptor substrates (IRSs) play central roles in
insulin/insulin-like growth factor (IGF) signaling and mediate a variety of their bioactivities
Ahrén et al., Acta Diabetol Lat 1981 :
CCK-39 potentiated glucose- as well as carbachol
induced insulin secretion, whereas it did not influence L-IPNA induced
insulin release
Velasquez-Mieyer et al., Int J Obes Relat Metab Disord 2003 (Obesity) :
With a similar WBISI, AAs had significantly higher CIR ( 30 ) ( 2.3+/-0.4 vs 1.01+/-0.1 ),
insulin response ( IAUC : 23 974+/-4828 vs 14 478+/-1463 ), and lower
insulin clearance ( 0.07+/-0.01 vs 0.11+/-0.01 ) than C ( all, P < 0.01 )
Zhao et al., Proc Natl Acad Sci U S A 1997 :
In this model, increased
insulin secretion in vivo will stimulate IGF-1 synthesis by the liver, and the secreted IGF-1 in turn feedback
inhibits insulin secretion from the beta cells through an IGF-1 receptor mediated pathway
Simpson et al., Pancreas 1995 :
Inhibition of cAMP metabolism with 1 mM MDL 12,330A ( RMI ) reduced
insulin synthesis stimulated by glucose and completely
inhibited insulin synthesis stimulated by theophylline
Chiu et al., Pancreas 2003 (Insulin Resistance) :
Insulin sensitivity index (ISI) , 1st phase
insulin response ( 1stIR ), and 2nd phase insulin response ( 2ndIR ) were assessed in 60 glucose tolerant subjects using hyperglycemic clamps
Pannacciulli et al., Obesity (Silver Spring) 2007 (Weight Gain) :
Total and incremental glucose AUCs during the OGTT ( but not the MT ) were negatively associated with BW change ( total, percent, and annual ), both before and after adjusting for sex, age, initial BW, follow-up time,
insulin action, RMR, fasting plasma glucose and insulin concentrations, and
insulin response
Paolisso et al., J Clin Endocrinol Metab 1988 (Diabetes Mellitus, Type 2) :
Continuous
insulin infusion
resulted in steady plasma
insulin levels, averaging 86 pmol/L, while during intermittent insulin administration plasma insulin levels were 5.7 and 158 pmol/L before and 3 min after the start of the insulin injection, respectively
Stefan et al., Diabetes 2003 (Diabetes Mellitus...) :
A subgroup of nondiabetic full-heritage Pima Indians ( n = 233 ) had measurements of body composition, glucose tolerance,
insulin action ( M ), endogenous glucose production ( EGP ; hyperinsulinemic clamp ), acute
insulin response ( AIR, 25-g intravenous glucose tolerance test, n = 118 normal glucose-tolerant subjects ), and percutaneous fat biopsy specimens from the periumbilical region ( n = 160 )
Qi et al., Am J Physiol Endocrinol Metab 2010 :
These data demonstrate that FAs differently regulate amylin and
insulin expression and
induce both amylin and
insulin release
Tokuyama et al., Diabetes Res Clin Pract 2001 (Diabetes Mellitus, Type 1...) :
Several therapeutic trials revealed that ( 1 ) intravenous regular insulin improved her metabolic control ; ( 2 ) continuous subcutaneous infusion ( CSII ) treatment with regular insulin or insulin lispro caused hyperglycemic period with hypoinsulinemia and hypoglycemic period with hyperinsulinemia alternately ; ( 3 ) adding heparin to insulin lispro in CSII resulted in dramatic increase of serum insulin level and improvement of glycemic control ; and ( 4 ) regular
insulin plus heparin in CSII could not
increase serum
insulin level and thus the glycemic values was not improved
Lee et al., Experimental biology and medicine (Maywood, N.J.) 2003 :
Stimulation of
insulin secretion with GLP-1, forskolin ( an activator of adenylyl cyclase ), or IBMX ( an inhibitor of PDE ) did not cause hypersecretion of insulin from islets of young Lep ( ob ) /Lep ( ob ) mice, and leptin did not
inhibit GLP-1 induced
insulin secretion from islets of these mice
Li et al., Diabetes Care 2001 (Birth Weight...) :
Among children with LBW, there were significant differences in fasting insulin,
insulin sensitivity, acute
insulin response , and HDL cholesterol between Caucasians and African-Americans
Benomar et al., Diabetes 2013 (Insulin Resistance) :
Central resistin treatment inhibited
insulin dependent phosphorylation of
insulin receptor (IR) , AKT, and extracellular signal related kinase 1/2 associated with reduced IR expression and with upregulation of suppressor of cytokine signaling-3 and phosphotyrosine phosphatase 1B, two negative regulators of insulin signaling
Shibata et al., J Pharmacol Sci 2013 (Diabetes Mellitus, Type 2...) :
Serine phosphorylation of
insulin receptor substrate (IRS)-1 negatively
regulates insulin signaling
Allon et al., Fertil Steril 2005 (Chronic Disease...) :
The administration of testosterone did not alter serum
insulin , and ICV
insulin did not
increase testosterone levels