糖尿病时由于胰岛素分泌不足，葡萄糖不能进入细胞进行葡萄糖有氧氧化、同时

During diabetes, due to insufficient insulin secretion, glucose cannot enter cells for aerobic oxidation of glucose, and at the same time it cannot inhibit the glucose xenobiotic pathway, that is, the main path of glucose in the blood disappears, while glucose in vivo production and excessive food intake due to increased food intake, Causes blood sugar to rise. <br>Insulin can promote the uptake of glucose through GLUT4 by muscles and adipose tissue, reduce cAMP levels by activating phosphodiesterase, activate glycogen synthase and inhibit phosphorylase, thereby accelerating glycogen synthesis, inhibiting glycogen decomposition, and It can activate the pyruvate dehydrogenase complex by activating pyruvate dehydrogenase phosphatase, accelerate the aerobic oxidation of sugar, inhibit gluconeogenesis in the liver, and increase the supply of acetyl CoA and NADPH, the decomposition products of sugar, in favor of this Synthesis of fatty acids as raw materials. Therefore, insulin has the effect of lowering blood sugar. Insufficient insulin secretion or lack of insulin receptors often leads to an increase in blood sugar; if the renal glucose threshold is exceeded, sugar is excreted from the urine, causing diabetes.

When diabetes due to insufficient insulin secretion, glucose can not enter the cells for glucose aerobic oxidation, at the same time can not inhibit the glucose heterogenous pathway, that is, the main way of glucose in the blood disappear, and glucose production and excessive food caused by the increase in intake of in vitro glucose, causing elevated blood sugar.<br>Insulin can promote muscle, adipose tissue, etc. through gluT4 glucose intake, by activating phosphodiesterase and reduce cAMP levels, so that glycogen assase is activated, phosphatase is inhibited, thus accelerating glycogen synthesis, inhibiting glycogen decomposition, but also by activating Acetone dehydrogenase phosphatase and the acrylate dehydrogenase complex to activate, accelerate the oxidation of sugar, inhibit the liver sugar isomorphism, sugar decomposition productaceyl CoA and NADPH supply increased, is conducive to the synthesis of fatty acids as a raw material. Therefore, insulin has the effect of lowering blood sugar. Inadequate insulin secretion or lack of insulin receptors often leads to elevated blood sugar, and if the renal sugar threshold is exceeded, the sugar is excreted from the urine, causing glycuria.

In diabetes, due to insufficient insulin secretion, glucose can not enter the cells for glucose aerobic oxidation, and can not inhibit the gluconeogenesis pathway, that is, the main route of glucose in the blood disappears, and the in vitro glucose intake caused by glucose production in vivo and overeating increases, resulting in the increase of blood glucose.<br>Insulin can promote muscle and adipose tissue to absorb glucose through GLUT4, reduce cAMP level by activating phosphodiesterase, activate glycogen synthase and inhibit phosphorylase, thus accelerating glycogen synthesis, inhibiting glycogen decomposition, and activating pyruvate dehydrogenase complex by activating pyruvate dehydrogenase phospholipase, speeding up the aerobic oxidation of glucose and inhibiting glycosylation in liver The increased supply of acetyl CoA and NADPH, the decomposition products of raw and sugar, is conducive to the synthesis of fatty acids. Therefore, insulin can reduce blood glucose. Insufficiencies of insulin secretion or insulin receptor often lead to hyperglycemia; if the renal glucose threshold is exceeded, the glucose is excreted from the urine, causing diabetes.