Peripheral glucose utilization

Peripheral glucose utilization describes the uptake and metabolism of glucose by tissues outside the central nervous system, primarily muscle, adipose tissue, and liver. These tissues require insulin to stimulate glucose uptake (except for some tissues such as brain and liver, which can uptake glucose independently). Enzymes like hexokinase and glucose transporters facilitate the cellular uptake and catabolism of glucose. Disrupted peripheral glucose utilization, as seen in insulin resistance, contributes to hyperglycemia in diabetes and plays a central role in metabolic disorders[1][3][4]. Peripheral pathways are regulated hormonally (mainly by insulin and glucagon) and neurally via the autonomic nervous system[1][2]. In summary, peripheral glucose utilization should not be treated as a receptor, protein, or canonical drug target, but rather as a physiological process involving numerous molecular components and regulatory mechanisms[3][4]. If you require structured data for a specific molecular target within this pathway (e.g., “insulin receptor” or “GLUT4”), please specify.

Other names

glucose uptakeglucose disposalglucose metabolism in peripheral tissues

Enhance peripheral glucose uptake (e.g., insulin); Increase insulin sensitivity (e.g., thiazolidinediones); Reduce hepatic glucose production (e.g., metformin); Promote glucose excretion (e.g., SGLT2 inhibitors)