Possible Correlation between Glucagon & Glucagon-Like Peptide 1 (GLP-1) with Type 2 Diabetic and Heart Failure

Abstract

Background: The history of glucagon started in 1920s when Kimball and Murlin stated that a circulating molecule with an impact on glucose homeostasis oppose the insulin effect is present. The glycogenolytic, ketogenic and gluconeogenic effects of glucagon were demonstrated in dogs at first. Shortly after glucagon was refined and sequenced at Eli Lilly (IN, USA), and constructed commercially by the company for treatment of insulin-induced hypoglycemia. Classically, the pathogenesis of T2DM is centralized on insulin resistance and β cell dysfunction; however the inappropriately raised α -cell function and resultant hyperglucagonemia have long been identified as a supporter of hyperglycemia in diabetic patients by promoting glucose production by the liver. Glucagon’s positive inotropic and chronotropic impacts were first shown in the isolated heart of cats, guinea pigs, rats, and dogs and were thereafter proved in vivo in humans. Although several hormones might be involved in postprandial insulin secretion, most of the incretin effect can be explained by increases in glucose dependant insulinotropic peptide so-called  gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1). GLP-1 is secreted from the intestinal L cells that are located with increasing density from the duodenum to the colon. Agonists of the GLP-1 receptor improve glycemic control via both their acute insulinotropic action and, under certain circumstances, also by chronic action to preserve β-cell mass through stimulation of β-cell proliferation and inhibition of apoptosis. Endothelial dysfunction is a common co-morbidity associated with insulin resistance and T2DM. Treatment of type-2 diabetic patients that present coronary artery disease with GLP-1 improves endothelial function without affecting insulin resistance.