It is a hypoglycemic drug that improves blood sugar tolerance in patients with type 2 diabetes and reduces basal and postprandial blood sugar. It can reduce the production of glycogen, reduce intestinal absorption of sugar, and increase insulin sensitivity by increasing peripheral sugar uptake and utilization. Unlike sulfonylurea drugs, metformin hydrochloride does not cause hypoglycemia in patients with type 8 diabetes or patients with normal blood sugar (except in special circumstances). After treatment, insulin secretion remains unchanged, while fasting insulin levels and daily plasma insulin levels are reduced.

This product is a hypoglycemic drug. Its pharmacological effects include: ① increasing the sensitivity of peripheral tissues to insulin and increasing insulin-mediated glucose utilization; ② increasing the utilization of glucose by non-insulin-dependent tissues, such as the brain, blood cells, renal medulla, intestines, skin, etc.; ③ inhibiting hepatic gluconeogenesis and reducing hepatic glucose output; ④ inhibiting intestinal wall cells from taking up glucose; ⑤ inhibiting the biosynthesis and storage of cholesterol and reducing blood triglyceride and total cholesterol levels. Unlike the effect of insulin, this product has no effect of promoting fat synthesis, no obvious hypoglycemic effect on normal people, and generally does not cause hypoglycemia when used alone for type 2 diabetes.

1. This product is a second-generation sulfonylurea antidiabetic drug, which is effective for most patients with type 2 diabetes. It can reduce fasting and postprandial blood sugar and reduce glycosylated hemoglobin (HbAlc) by 1% to 2%. 2. The main function of this type of drug is to stimulate pancreatic b cells to secrete insulin, but the prerequisite is that pancreatic b cells still have a certain function of synthesizing and secreting insulin. 3. Its mechanism is to specifically bind to the sulfonylurea receptor on the b cell membrane, thereby closing the K channel, causing changes in membrane potential, opening the Ca2 channel, and increasing intracellular Ca2, which promotes insulin secretion. 4. In addition, there are extra-pancreatic effects, including improving the insulin resistance of peripheral tissues (such as liver, muscle, and fat).

1. Stimulate the pancreatic islet beta cells to secrete insulin, which presupposes that the islet beta cells also have a certain ability to synthesize and secrete insulin. 2. By increasing portal vein insulin levels or acting directly on the liver, inhibiting liver glycogenolysis and gluconeogenesis, the liver produces and outputs less glucose. 3. It may also increase the sensitivity of extrapancreatic tissues to insulin and the utilization of sugar (probably mainly through post-receptor effects). Therefore, the overall effect is to reduce fasting blood sugar and postprandial blood sugar.

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