Young A, Pittner R, Gedulin B, Vine W, Rink T
Amylin Pharmaceuticals, San Diego, CA 91901, USA.
Biochem Soc Trans. 1995 May;23(2):325-31. doi: 10.1042/bst0230325.
This review describes how amylin may work in the control of carbohydrate metabolism by actions on gastric emptying and on muscle glycogen metabolism. Amylin, which is co-secreted with insulin from pancreatic beta-cells in response to nutrient stimuli, affects both carbohydrate absorption and carbohydrate disposal. Amylin appears to regulate carbohydrate metabolism as a partner to insulin. Defending fuel stores tends to be hierarchical; plasma glucose is defended first, then muscle glycogen, then liver glycogen, then fat. Fuel stores are replenished by both incorporating ingested nutrient and by translocating nutrient stores among body sites. Lactate may better be regarded as a vector of fuel transfer rather than a 'dead end' in metabolism. Amylin can promote the translocation of lactate from muscle to liver. The amylin effect, illustrated by the simultaneous decrease in muscle glycogen and increase in liver glycogen [53, 56], is similar to the catecholamine effect observed by Cori et al. [57]. Amylin thus may be important in maintaining liver glycogen stores via the Cori cycle and the 'indirect' glycogen synthesis pathway [58,59]. Unlike catecholamines, amylin does not mobilize fat or impede insulin action in adipose tissue [30,35]. It can supply lactate to the liver, and because lactate is a preferred lipogenic substrate [60], may thereby favour fat storage. Amylin may also help to control carbohydrate absorption via an 'entero-insular loop' to ensure that absorption from the gut remains within the regulatory limits for carbohydrate disposal by peripheral tissues. This regulatory system is essential for normal control of plasma glucose and appears to be disrupted in type-1 diabetes, an amylin-deficient state.
本综述描述了胰淀素如何通过作用于胃排空和肌肉糖原代谢来调控碳水化合物代谢。胰淀素与胰岛素一起由胰腺β细胞在营养刺激下共同分泌，它会影响碳水化合物的吸收和处理。胰淀素似乎作为胰岛素的协同因子来调节碳水化合物代谢。维持燃料储备往往具有层级性：首先维持血糖水平，然后是肌肉糖原，接着是肝糖原，最后是脂肪。通过摄入营养物质以及在身体各部位之间转移营养储备来补充燃料储备。乳酸或许更应被视为一种燃料转移载体，而非代谢中的“终产物”。胰淀素可促进乳酸从肌肉向肝脏的转运。胰淀素的作用表现为肌肉糖原同时减少而肝糖原增加[53, 56]，这与科里等人[57]观察到的儿茶酚胺效应相似。因此，胰淀素可能通过科里循环和“间接”糖原合成途径[58, 59]在维持肝糖原储备方面发挥重要作用。与儿茶酚胺不同，胰淀素不会动员脂肪或阻碍胰岛素在脂肪组织中的作用[30, 35]。它能为肝脏提供乳酸，并且由于乳酸是一种优质的生脂底物[60]，可能因此有利于脂肪储存。胰淀素还可能通过“肠 - 胰岛轴”帮助控制碳水化合物吸收，以确保肠道吸收保持在周围组织处理碳水化合物的调节范围内。这种调节系统对于正常控制血糖至关重要，而在1型糖尿病（一种胰淀素缺乏状态）中似乎受到破坏。
