INSULIN, GLUCAGON, AND SOMATOSTATIN IN NORMAL PHYSIOLOGY AND DIABETES-MELLITUS
INSULIN, GLUCAGON, AND SOMATOSTATIN IN NORMAL PHYSIOLOGY AND DIABETES-MELLITUS
复制标题
DOI：
10.2337/diabetes.25.12.1091
复制
发表时间：
1976-01-01
期刊：
影响因子：
7.7
通讯作者：
HENDLER, R
中科院分区：
文献类型：
--
作者：
FELIG, P;WAHREN, J;HENDLER, R
本文综述了胰岛素和胰高血糖素在正常生理和糖尿病中的作用。在正常人中，葡萄糖摄入伴随着胰岛素的升高和胰高血糖素的下降，并且主要在肝脏中处理，肝脏是对这两种激素敏感的器官。以生理量输注胰高血糖素表明，胰岛素分泌而不是胰高血糖素抑制是决定葡萄糖处置的主要因素。血糖的轻微升高引起胰岛素浓度的增加，并在血浆胰高血糖素不发生变化的情况下抑制肝脏葡萄糖输出。胰高血糖素的主要生理作用是预防低血糖，否则低血糖会伴随非碳水化合物（蛋白质）介导的胰岛素分泌。在糖尿病和正常患者中，胰高血糖素对肝葡萄糖产生的刺激作用是短暂的。胰高血糖素升高或I/G [胰岛素/胰高血糖素]比值改变可导致葡萄糖耐量或糖尿病控制恶化，但前提是存在绝对胰岛素缺乏或胰高血糖素药理学升高。在施用生长抑素后，正常受试者中的长期低胰岛素血症导致在基础胰高血糖素分泌缺乏的情况下的空腹高血糖症。在糖尿病患者中，生长抑素产生的餐后高血糖的改善可以通过其对胃肠道中碳水化合物吸收的抑制作用来解释。胰岛素缺乏是糖尿病的主要病理生理障碍。虽然胰高血糖素可能会加重胰岛素缺乏的后果，但它对糖尿病的发展既不充分也不必要。
Studies are reviewed in which the roles of insulin and glucagon in normal physiology and in diabetes are examined. In normal man, glucose ingestion is accompanied by a rise in insulin and fall in glucagon and is primarily disposed of in the liver, an organ sensitive to both hormones. Infusions of glucagon in physiologic amounts indicate that insulin secretion rather than glucagon inhibition is the primary factor determining glucose disposal. Minor elevations in blood glucose elicit increments in insulin concentration and inhibition of hepatic glucose output in the absence of changes in plasma glucagon. The primary physiologic role of glucagon is to prevent the hypoglycemia that would otherwise accompany noncarbohydrate(protein)-mediated insulin secretion. In diabetic and normal patients the stimulatory effect of glucagon on hepatic glucose production is evanescent. Increases in glucagon or changes in the I/G [insulin/glucagon] ratio can bring about deterioration in glucose tolerance or in diabetic control only so long as absolute insulin deficiency is present or pharmacologic elevations in glucagon are produced. After somatostatin administration, prolonged hypoinsulinemia in normal subjects results in fasting hyperglycemia in the absence of basal glucagon secretion. In diabetic patients the improvement in postprandial hyperglycemia produced by somatostatin can be accounted for by its inhibitory action on carbohydrate absorption in the gastrointestinal tract. Insulin deficiency is the primary pathophysiologic disturbance in diabetes. While glucagon may worsen the consequences of insulin lack, it is neither sufficient nor necessary for the development of diabetes.