The Utilization of Incretin Mimetics and DPPIV Inhibitors in the Essay

The Utilization of Incretin Mimetics and DPPIV Inhibitors in the Management of Type II Diabetes Mellitus - Essay ExampleThe initial results obtained from clinical trials with these upstart agents indicate a very high promise of achieving better blood glucose control by adding them to the therapeutic arsenal for the management of type 2 diabetes mellitus.Incretin mimetics ar a new class of antidiabetic agents with multiple blood sugar lowering actions that mimic the actions of incretin hormones. Incretins argon peptide hormones that originate in the gastrointestinal tract. The two major incretins in reality argon glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP). These hormones are released during nutrient absorption, when they serve to potentiate the secretion of insulin(Nielsen) Although both GLP-1 and GIP act as incretin hormones in normal subjects, only GLP-1 can be used to treat DM2 because diabetes is often associated with a blunted or absent response to GIP. It has been shown that whereas GLP-1 levels are significantly decreased in DM2, GIP values are normal,suggesting that DM2 patients are resistant to the biological effects of GIP, rendering it relatively ineffective (2A)In mammals, GLP-1 is derived from the proglucagon peptide in mucosal L-cells of the small intestine(Drucker Glucagon-Like Peptides)DDipeptidyl peptidase (DPP-IV) extends the bioavailability of many peptides by suppressing their break-down. Several incretin mimetics and DPP-IV inhibitors are undergoing late-stage clinical trials for the treatment of type 2 diabetes and results so far have shown some promises. Their mechanisms of action include enhancement of glucose-dependent insulin secretion suppression of inappropriately fantastic glucagon secretion slowing of gastric emptying and appetite suppression(Nielsen). Type 2 diabetes is characterized by the emergence of postprandial (post meal) and, subsequently, fasting hyperglycemia (fasting plasma glu cose 125 mg/dl) (Nielsen Drucker Glucagon-Like Peptides). hyperglycaemia results from pancreatic -cells secreting inadequate insulin to compensate for insulin-resistance in peripheral tissues(Porte and Sherwin Weyer). Only about 33 percent of type 2 diabetes mellitus patients in the United States are satisfactory to achieve the 7% HbA1c recommended by the American Diabetes Association. However, after the administration of incretin mimetics and DPP-IV inhibitors on some of these patients, there is a significant improvement in their glycemic profile. Their after-meal blood glucose level, and subsequently their HbA1c were better(Freeman). Despite exercise, diet control and some pharmacological intervention in patients with DM 2, control of blood sugar has become increasingly difficult, especially in patients who had been on long term therapy. The progressive deterioration of the beta-cells of the pancreas, which in turn causes deficient insulin (as well as increased glucagon producti on) is responsible for this failure of treatment. The incretin mimetics and DPP IV inhibitors are thought to offer hope in improving the glycemic profile of patients because they act primarily to both increase