Arner P, Bolinder J, Ostman J
J Clin Invest. 1983 Mar;71(3):709-14. doi: 10.1172/jci110817.
The effect of glucose ingestion on insulin action was investigated in isolated human fat cells. Subcutaneous adipose tissue was obtained from eight normal adult volunteers before and 1 h after oral intake of 100 g of glucose. Lipolysis (glycerol release) and specific insulin receptor binding were determined. Insulin binding increased significantly by 20-30% after glucose ingestion. This was due to an increase in insulin binding affinity, without any change in the receptor number. The concentration of insulin producing half-maximum inhibition (ED(50)) of basal lipolysis was 50 muU/ml before and 0.25 muU/ml after glucose ingestion (P < 0.01), which represented a 200-fold difference. As regards isoprenaline-induced lipolysis, the ED(50) for insulin inhibition was 30 muU/ml before and 2.5 muU/ml after oral glucose (P < 0.01), which was a 12-fold difference. The maximum insulin-induced inhibition of basal and isoprenaline-induced lipolysis were not altered after oral glucose. It is concluded that glucose ingestion is accompanied by a marked increase in insulin sensitivity of human fat cells and this may be an important modulating factor in the overall scheme of insulin action.
在分离的人脂肪细胞中研究了葡萄糖摄入对胰岛素作用的影响。从8名正常成年志愿者身上获取皮下脂肪组织,分别在口服100克葡萄糖之前和之后1小时进行。测定了脂解作用(甘油释放)和特异性胰岛素受体结合情况。葡萄糖摄入后,胰岛素结合显著增加了20%-30%。这是由于胰岛素结合亲和力增加,而受体数量没有任何变化。基础脂解作用产生半数最大抑制(ED(50))的胰岛素浓度在葡萄糖摄入前为50 μU/ml,摄入后为0.25 μU/ml(P < 0.01),相差200倍。至于异丙肾上腺素诱导的脂解作用,胰岛素抑制的ED(50)在口服葡萄糖前为30 μU/ml,口服后为2.5 μU/ml(P < 0.01),相差12倍。口服葡萄糖后,胰岛素对基础脂解作用和异丙肾上腺素诱导的脂解作用的最大抑制作用没有改变。结论是,葡萄糖摄入伴随着人脂肪细胞胰岛素敏感性的显著增加,这可能是胰岛素作用总体机制中的一个重要调节因素。