Gene interactions and pathways from curated databases and text-mining
J Clin Endocrinol Metab 2011, PMID: 21346060

Cardioprotective effects of glucose and insulin administration while maintaining normoglycemia (GIN therapy) in patients undergoing coronary artery bypass grafting.

Carvalho, George; Pelletier, Patricia; Albacker, Turki; Lachapelle, Kevin; Joanisse, Denis R; Hatzakorzian, Roupen; Lattermann, Ralph; Sato, Hiroaki; Marette, André; Schricker, Thomas


Coronary artery bypass grafting (CABG) is complicated by ischemia-reperfusion injury jeopardizing myocyte survival.


The aim of the study was to investigate whether glucose and insulin administration, while maintaining normoglycemia (GIN therapy) using a hyperinsulinemic-normoglycemic clamp technique, is cardioprotective in patients undergoing CABG.


We conducted a randomized controlled trial at a tertiary care university teaching hospital.


We studied 99 patients undergoing elective CABG.


Patients were randomly assigned to receive either GIN from the beginning of surgery until 24 h after CABG (GIN, n = 49) or standard metabolic care (control, n = 50).


We measured plasma concentrations of cardiac troponin I and free fatty acids, cardiac function as assessed by transesophageal echocardiography, glycogen content, glycogen synthase activity, and the expression of AMP-activated protein kinase (AMPK) and protein kinase B (AKT) in cardiomyocytes.


Patients receiving GIN therapy showed an attenuated release of cardiac troponin I (P < 0.05) and improved myocardial function (P < 0.05). Systemic free fatty acid concentrations were suppressed (P < 0.05), whereas intracellular glycogen content and glycogen synthase activity were not altered. The AMPK activity remained unchanged during ischemia in the GIN group, whereas it increased in the control group (P < 0.05). Enhanced AKT phosphorylation before ischemia was observed (P < 0.05) in the presence of GIN. However, there was no evidence for AKT-dependent AMPK inhibition.


GIN therapy protects the myocardium and inhibits ischemia-induced AMPK activation.

Diseases/Pathways annotated by Medline MESH: Myocardial Reperfusion Injury, Postoperative Complications
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Text Mining Data

AMPK ⊣ AKT: " However, there was no evidence for AKT dependent AMPK inhibition "

Manually curated Databases

No curated data.