Endocrine Abstracts

GLP-1 stimulates β-cell proliferation, it also enhances the differentiation of new beta cells from progenitor cells in the pancreatic duct epithelium and it is capable of inhibiting apoptosis of β cells. GLP-1 also exhibits other effects of importance for glucose homeostasis, such as, inhibiting glucagon secretion, delaying gastric emptying, and stimulating insulin biosynthesis. These effects come along with a potential increase in peripheral insulin action. Type 2 diabetic patients have an impaired secretion of GLP-1. On the other hand, patients with type 2 diabetes mellitus are considered to be at high risk for cardiovascular disease. A mutual relationship exists between insulin resistance and heart failure. High affinity receptors for GLP-1 are present in the heart and vascular tissue, so it is conceivable that the incretins may improve cardiovascular function.

Aim: The aim of this study was To assess the plasma level of GLP-1 in patients with congestive heart failure, both those with type 2 diabetes mellitus and those who are non diabetic and to assess the possible role of GLP-1 in the development of congestive heart failure.

Method: Our study included 54 subjects, divided into 4 groups; ‘group 1’ included 15 non diabetic patients with congestive heart failure, ‘group 2’ included 15 type 2 diabetic patients with congestive heart failure, ‘group 3’ included 12 type 2 diabetic patients with normal cardiac function and ‘group 4’ included 12 normal control subjects. All subjects were submitted to full clinical and biochemical assessment, Fasting plasma glucagon-like peptide 1 measured by ELISA and echocardiogram.

Results: In the presenting study fasting serum GLP-1 was found to be significantly lower in cases suffering of either heart failure or type 2 DM in comparison to those healthy control cases. Furthermore, diabetic cases with heart failure showed significant lower level of serum GLP-1 in comparison to non-diabetic heart failure cases. Therefore, our results may suggest a role for GLP-1 deficiency in development of congestive heart failure either in type 2 diabetic or non-diabetic cases.