![]() The above processes lead to a decrease in blood glucose, managing type II diabetes and exerting positive effects on glycemic control.Īfter ingestion, the organic cation transporter-1 (OCT1) is responsible for the uptake of metformin into hepatocytes (liver cells). It is well established that metformin inhibits mitochondrial complex I activity, and it has since been generally postulated that its potent antidiabetic effects occur through this mechanism. Preform decreases blood glucose levels by decreasing hepatic glucose production (gluconeogenesis), decreasing the intestinal absorption of glucose, and increasing insulin sensitivity by increasing peripheral glucose uptake and utilization. ![]() Preform's mechanisms of action are unique from other classes of oral antihyperglycemic drugs. In contrast with drugs of the sulfonylurea class, which lead to hyperinsulinemia, the secretion of insulin is unchanged with metformin use. Preform reduces liver (hepatic) production of glucose, decreases the intestinal absorption of glucose, and enhances insulin sensitivity by increasing both peripheral glucose uptake and utilization. In patients diagnosed with type 2 diabetes, insulin no longer exerts adequate effects on tissues and cells (called insulin resistance) and insulin deficiency may also be present. Type II diabetes is characterized by a decrease in sensitivity to insulin, resulting in eventual elevations in blood glucose when the pancreas can no longer compensate. Insulin is an important hormone that regulates blood glucose levels. With metformin therapy, insulin secretion remains unchanged while fasting insulin levels and daylong plasma insulin response may actually decrease. Unlike sulfonylureas, metformin does not produce hypoglycemia in either patients with type 2 diabetes or normal subjects and does not cause hyperinsulinemia. This has been shown at therapeutic doses in controlled, medium-term or long-term clinical studies: Preform reduces total cholesterol, LDL, cholesterol and triglycerides levels. In humans, independently of its action on glycemia, metformin has favorable effects on lipid metabolism. Preform increases the transport capacity of all types of membrane glucose transporters (GLUTs) known to date. Preform also delays intestinal glucose absorption. In muscle, it increases insulin sensitivity, improving peripheral glucose uptake and utilization. Preform reduces hepatic glucose production by inhibiting gluconeogenesis and glycogenolysis, and stimulates intracellular glycogen synthesis by acting on glycogen synthase. Preform is an antihyperglycemic agent which improves glucose tolerance in patients with type 2 diabetes, lowering both basal and postprandial plasma glucose.
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