Insulin 产品

Upon nutrient ingestion, particularly carbohydrates, ensuing elevated blood glucose levels trigger the release of insulin into the bloodstream. This hormone engages specific transmembrane receptors situated on target cells, namely myocytes, adipocytes, and hepatocytes.

Insulin's foremost role involves the facilitation of facilitated diffusion of glucose across cell membranes. This translocation of glucose from the extracellular milieu to the intracellular compartment facilitates its utilization as an energy substrate, predominantly discernible in muscle cells engaged in contractile activities.

Furthermore, insulin encourages glycogenesis, a process where surplus glucose is stored in the form of glycogen in hepatic and skeletal muscle cells. This endows the body with a readily mobilizable reservoir of glucose, crucial during times of heightened energy demands.

In tandem with its glycemic control functions, insulin curtails gluconeogenesis, the hepatic synthesis of glucose from non-carbohydrate precursors. By curtailing this gluconeogenic pathway, insulin safeguards against unwarranted glucose production and the concomitant elevation of blood glucose levels.

Insulin's regulatory purview extends to lipid metabolism. During periods of elevated insulin concentrations, as observed postprandially, adipocytes display an increased propensity to absorb free fatty acids and convert them into triglycerides for storage in adipose tissue depots. This, in turn, mitigates circulating fatty acid levels, averting lipotoxicity.

In addition to its cardinal involvement in carbohydrate and lipid metabolism, insulin actively influences protein metabolism. By augmenting cellular amino acid uptake, insulin provides substrates for protein synthesis, thereby contributing to tissue growth, repair, and overall nitrogen balance.

Disruptions in insulin signaling can manifest as insulin resistance, characterized by diminished cellular responsiveness to insulin's actions. This aberration is intricately linked to the pathophysiology of type 2 diabetes mellitus. Conversely, in type 1 diabetes mellitus, pancreatic beta cell dysfunction results in an absolute insulin deficiency, necessitating exogenous insulin administration for glycemic regulation.