الفهرس 
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Abstract
Glucagon-like peptide-1 (GLP-1) is an incretin hormone secreated by L cells of the GIT in response to nutrient intake and plays a major role in glucose homeostasis by stimulating insulin secretion, suppressing glucagon secretion, inhibiting gastric emptying, and reducing appetite and food intake. This hormone exerts its effects through interaction with G-protein coupled receptors. The GLP-1 receptor is widely expressed throughout the body (α- and β-cells in the islets of pancreas, other parts of the gastrointestinal tract, central and peripheral nervous systems, heart, kidney, and the lung).
In patients with type 2 diabetes mellitus, the incretin effect is reduced or even absent due to significant, reduction in meal-stimulated levels of GLP-1. Therapeutic efforts have been focused on the development of GLP-1 receptor agonists, which would appear to be ideal therapeutic agents for use in patient with type 2 diabetes. Incretin mimetics, exenatide and liraglutide, which are GLP-1 receptor agonists resistant to DPP-IV degradation, and the DPP-IV inhibitors (the gliptins), which potentiate the effect of the endogenously secreted incretin hormones by competitively inhibiting the enzyme responsible for their degradation The incretin mimitics have effects extending beyond their known ability to lower glucose. These include trophic effects on the β-cell; reduce postprandial lipemia; lower blood pressure; improve myocardial contractility and endothelial function; and potential neuroprotective, neurotrophic, and bone resorptive effects. The ability of GLP-1 receptor agonists to improve myocardial contractility and endothelial function and favorably affect blood pressure and lipids in the context of weight loss has the potential to ameliorate some of the premature cardiovascular burden in patients with diabetes Ischemic Heart Disease (IHD) is a clinical syndrome characterized by decreased oxgen supply to myocardial muscle mainly due to coronary atherosclerosis, the earliest event in atherogenesis is endothelial dysfunction manifested as deficiencies of nitric oxide (NO) and prostacyclin. This can be induced by various noxious insults including dyslipidemia, diabetes, hypertension, smooking. Recent data suggest that the prediabetic state may be associated with endothelial dysfunction possibly due to IR and inflammation.
Both T2DM and IHD charcterized by IR and inflammation. In summary, IHD is increased in diabetes due to many traditional and nontraditional risk factors. The latter have recently been recognized to have a significant role in the initiation and the progression of atherosclerosis, over its long natural history from endothelial function to clinical events. The aim of this study was to clarify the relation between T2DM, IHD and fasting plasma GLP-1. This study was conducted on 54 subjects;
15 of them were ischemic and type2 diabetics, 15 were ischemic non diabetics, 12 were type 2 diabetics non ischemic and 12 were normal (control).
In conclusions; the present study revealed that:
§ Fasting plasma GLP-1 was found to be significantly lower in T2DM and IHD than control subjects.
§ Patients with IHD associated with T2DM showed more decrease in fasting level of GLP-1 than patients with IHD or T2DM alone.
§ Fasting plasma GLP-1 was indirectly and significantly correlated with HbA1C, and diastolic blood pressure in all studied groups.
§ Hemoglobin A1C (HbA1C) was the most important predictor of fasting plasma GLP-1 among the studied parameters followed by low density lipoproteins (LDL).