Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Manitoba, A210 - 753 McDermot Avenue, Winnipeg, MB R3E 0T6, Canada.
Can J Physiol Pharmacol. 2013 Feb;91(2):91-100. doi: 10.1139/cjpp-2012-0228. Epub 2013 Feb 11.
The augmented whole-body glucose uptake response to insulin during the postprandial state is described as meal-induced insulin sensitization (MIS). MIS occurs when the presence of food in the upper gastrointestinal tract activates 2 feeding signals (activation of hepatic parasympathetic nerves and elevation of hepatic glutathione level), and causes insulin to release hepatic insulin sensitizing substance (HISS), which stimulates glucose uptake in skeletal muscle, heart, and kidneys. HISS action results in nutrient storage, primarily as glycogen. Impairment of HISS release results in the absence of meal-induced insulin sensitization (AMIS), which causes postprandial hyperglycemia and hyperinsulinemia, and chronically leads to the progression to a cluster of metabolic, vascular, and cardiac dysfunctions, which we refer to as components of the AMIS syndrome. Manipulation of the MIS process in health and in disease, by pharmacological and nonpharmacological interventions, is outlined in this review. High fat or sugar supplemented diet reduces MIS; exercise elevates MIS; and antioxidants protect MIS against reductions associated with diet and age.
进食后全身葡萄糖摄取对胰岛素的增强反应被描述为餐后胰岛素敏感性增强(MIS)。当上消化道中的食物存在时,MIS 会激活 2 种进食信号(肝副交感神经的激活和肝谷胱甘肽水平的升高),并导致胰岛素释放肝胰岛素敏感物质(HISS),从而刺激骨骼肌、心脏和肾脏的葡萄糖摄取。HISS 作用导致营养物质的储存,主要是糖原。HISS 释放的损害会导致餐后胰岛素敏感性增强的缺失(AMIS),从而导致餐后高血糖和高胰岛素血症,并导致代谢、血管和心脏功能障碍的进展,我们称之为 AMIS 综合征的组成部分。本文综述了通过药理学和非药理学干预来调节健康和疾病中的 MIS 过程。高脂肪或高糖补充饮食会降低 MIS;运动可提高 MIS;抗氧化剂可防止与饮食和年龄相关的 MIS 减少。