The Therapeutic Options For Treating Type 2 Diabetes Mellitus

The therapeutic options for treating type 2 diabetes mellitus (T2DM) have been widened since April 2005 due to the introduction of Exenatide, the first incretin mimetic (Bond 2006). Due to the prevalence of this disease, the largest and most powerful pharmaceutical companies are ambitious to develop effective therapeutic methods. Exenatide is a synthetic peptide that was first identified in the saliva of Heloderma Suspectum, a species of venomous lizard native to areas in the United States and Mexico (Kalra 2013). In this review, the focus is on the mechanisms of exenatide and how these may relate to therapeutic responses . The exact mechanisms of Exenatide are continually under investigation with certain evaluations focusing on the†¦show more content†¦The synthetic preparation Exenatide targets the GLP-1 receptor (GLP-1R) and acts as an agonist which elicits action of the GLP-1 pathway while displaying other antihyperglycemic actions (McDougal, McKay Fisher 2011). Re actions of an active GLP-1 pathway typically lead to insulin secretion by the beta cells and the suppression of inadvertently elevated glucagon secretion (Iltz, 2006). The Active Pharmaceutical Ingredient (API), has been proven clinically to elicit favourable responses on patient; glucose-dependent insulin secretion, first-phase insulin response, glucagon secretion, gastric emptying and food intake (Derosa et.al, 2010). Exenatide preparations are made by incorporating molecules into a matrix of poly-D, L-lactide-co-glycolide which, although similar to the native glucagon-like peptide has a much longer duration of action (Kalra 2013). The finished dosage form is a pre-filled syringe, which contains the liquid dosage. The drug should be administered subcutaneously by injection, after a period of 60 minutes, prior to consuming morning and afternoon meals. These dosage times are critical for maintaining efficacy and clinical significance as the drug slows the rate of gastric emptying, reducing the rate of meal derived glucose (Bond 2006). Studies A study conducted by Buse et al (2007) examined the metabolic effects of 2 years of exenatide treatment in patients with T2DM. The results of their study showed HbA(1c) levels were