Differential tissue sensitivity to elevated endogenous insulin levels during experimental peritonitis in rats.
Differential tissue sensitivity to elevated endogenous insulin levels during experimental peritonitis in rats.
复制标题
大鼠实验性腹膜炎期间组织对内源性胰岛素水平升高的敏感性不同。
DOI：
10.1016/0026-0495(74)90075-4
复制
发表时间：
1974
期刊：
影响因子：
--
通讯作者：
George H. A. Clowes
中科院分区：
文献类型：
--
作者：
N.Thomas Ryan;George L. Blackburn;George H. A. Clowes
通过测定离体组织的胰岛素相关代谢与血胰岛素和底物水平的相关性，研究了大鼠实验性腹膜炎后葡萄糖代谢的紊乱。尽管血糖浓度大致相等，但感染禁食大鼠的血液胰岛素浓度是正常禁食对照大鼠的3倍，表明对胰岛素的降糖作用具有抵抗力。循环胰岛素增加与胰岛素敏感性脂肪组织丙酮酸脱氢酶复合物升高3倍，以及附睾脂肪垫碎片将葡萄糖转化为CO2的速率增加3倍相关。与禁食对照组相比，禁食感染动物的循环非酯化脂肪酸也减少，附睾脂肪组织消耗相对较少，这可能是由于胰岛素在对抗脂质动员方面的强效作用。相比之下，隔膜丙酮酸脱氢酶并未升高，隔膜葡萄糖转化为CO2也未因循环胰岛素升高而受到刺激。有人提出，减少脂肪动员，同时没有加速葡萄糖氧化的肌肉可能会导致肌肉代谢燃料不足，这可能会反过来，促进肌肉的氨基酸燃烧，以满足细胞的能量需求。这一机制可能为与严重感染相关的过量蛋白质催化剂提供了一个假设的生化解释。
Disturbances of glucose metabolism consequent to experimental peritonitis in rats were studied by measurement of insulin-related metabolism of isolated tissues in correlation with blood insulin and substrate levels. Blood insulin concentrations were threefold higher in infected fasting rats than in normal fasting controls, despite approximately equal blood glucose concentrations, suggesting resistance to the hypoglycemic action of insulin. The increased circulating insulin was associated with a threefold elevation of the insulin-sensitive adipose tissue pyruvate dehydrogenase enzyme complex, and a threefold increase in the rate of conversion of glucose to CO2by fragments of epididymal fat pads. Fasting infected animals also had reduced circulating nonesterified fatty acids and relatively less depletion of epididymal adipose tissue, when compared to fasted controls presumably due to the potent action of insulin in opposing lipid mobilization. In contrast, diaphragm pyruvate dehydrogenase was not elevated, nor was diaphragm glucose conversion to CO2stimulated in response to the elevated circulating insulin. It is proposed that reduced fat mobilization without concomitantly accelerated glucose oxidation by muscle may result in insufficient metabolic fuel for muscle and this may, in turn, promote amino acid combustion by muscle to meet cellular energy requirements. This suggested mechanism may provide a hypothetical biochemical explanation for the excessive protein catabolism associated with severe infection.