Young A A
Physiology Department, Amylin Pharmaceuticals, Inc., San Diego, California 92121.
J Cell Biochem. 1994;55 Suppl:12-8. doi: 10.1002/jcb.240550003.
The 37-amino acid amylin, co-secreted from the pancreatic beta cells with insulin in response to nutrient stimuli has actions in a number of tissues of metabolic interest. In muscle it opposes glycogen synthesis and activates glycogenolysis, an action likely to underly its stimulation of lactate flux. Amylin therefore appears to have the effect of transposing carbon from peripheral stores to the liver, where it is made available for hepatic synthesis of glucose, glycogen, and lipid. While amylin induces insulin resistance in skeletal muscle, it does not oppose insulin action in fat and may therefore favor fuel deposition in this tissue. Amylin acts on the beta cell to inhibit insulin secretion. Relative impairment of insulin secretion, muscle insulin resistance, relatively preserved insulin sensitivity in fat, increased lactate turnover, and increased hepatic glucose production are features of insulin resistance and early non-insulin-dependent diabetes mellitus. Amylin is elevated in these dysfunctional metabolic states and may be involved in their pathogenesis.
37个氨基酸的胰淀素与胰岛素一起从胰腺β细胞中共同分泌，以响应营养刺激，在许多具有代谢意义的组织中发挥作用。在肌肉中，它抑制糖原合成并激活糖原分解，这一作用可能是其刺激乳酸通量的基础。因此，胰淀素似乎具有将碳从外周储存转移到肝脏的作用，在肝脏中，碳可用于肝脏合成葡萄糖、糖原和脂质。虽然胰淀素会诱导骨骼肌中的胰岛素抵抗，但它并不拮抗脂肪中的胰岛素作用，因此可能有利于该组织中的燃料沉积。胰淀素作用于β细胞以抑制胰岛素分泌。胰岛素分泌相对受损、肌肉胰岛素抵抗、脂肪中胰岛素敏感性相对保留、乳酸周转增加以及肝葡萄糖生成增加是胰岛素抵抗和早期非胰岛素依赖型糖尿病的特征。在这些功能失调的代谢状态下，胰淀素水平升高，可能参与其发病机制。
