Glucoxit Mechanism of Action

Pharmacology: Pharmacodynamics: Metformin hydrochloride does not stimulate pancreatic beta cells of insulin; insulin secretion must be present for metformin to work properly. Metformin hydrochloride may increase the number and/or affinity of insulin receptors on cell surface membranes, especially at peripheral receptor sites, and help to correct down regulation of the insulin receptor. This effect increases the sensitivity to insulin at receptor and post receptor binding sites and increases uptake peripherally. Insulin concentrations remain unchanged or are slightly reduced as glucose metabolism improves. In addition, metformin's metabolic effects increase hepatic glycogen stores in diabetic patients (but not in non-diabetic patients). Decrease intestinal glucose absorption, and reduce fatty acid oxidation and acetyl co-enzyme A formation. Glucose uptake or free fatty acid oxidation is effects considered to be caused by non-insulin mediated mechanisms.
Pharmacokinetics: Metformin hydrochloride is absorbed over a period of 6 hours with bioavailability between 50%-60% under fasting condition. Presence of food will delay the absorption, lowers the peak concentration by 40% and decreases the bioavailability by 25%. Peak serum concentration at steady state is 1 to 2 mcg/ml, achieved within 2 hours. The main sites of concentration without accumulation are the intestinal mucosa and the salivary glands; also, the erythrocyte mass may be a compartment of distribution. It has a plasma half-life of about 3 hours and it is not bound to plasma proteins. Metformin hydrochloride does not undergo hepatic metabolism and up to 90% of a dose of metformin is excreted unchanged in the urine. About 30% of a dose is eliminated in the feces. Haemodialysis with a clearance of 170 ml/minute prevents accumulation of metformin.