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Vildagliptin + Metformin Hydrochloride
Vildagliptin acts primarily by inhibiting DPP-4, the enzyme responsible for the degradation of the incretin hormones GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic polypeptide). The administration of Vildagliptin results in a rapid and complete inhibition of DPP-4 activity resulting in increased fasting and postprandial endogenous levels of the incretin hormones GLP-1 and GIP. By increasing the endogenous levels of these incretin hormones, Vildagliptin enhances the sensitivity of beta cells to glucose, resulting in improved glucose-dependent insulin secretion. By increasing endogenous GLP-1 levels, Vildagliptin also enhances the sensitivity of alpha cells to glucose, resulting in more glucose-appropriate glucagon secretion. The enhanced increase in the insulin/glucagon ratio during hyperglycaemia due to increased incretin hormone levels results in a decrease in fasting and postprandial hepatic glucose production, leading to reduced glycaemia.
Metformin lowers both basal and postprandial plasma glucose. It does not stimulate insulin secretion and therefore does not produce hypoglycaemia or increased weight gain. Metformin may exert its glucose-lowering effect via four mechanisms:
- By reduction of hepatic glucose production through inhibition of gluconeogenesis and glycogenolysis
- In muscle, by modestly increasing insulin sensitivity, improving peripheral glucose uptake and utilisation.
- By delaying intestinal glucose absorption.
- Stimulates intracellular glycogen synthesis by acting on glycogen synthase and increases the transport capacity of glucose transporters (GLUT-1 and GLUT-4).