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质膜水平的信号转导缺陷导致胰岛素无法激活泌乳大鼠白色脂肪细胞中的丙酮酸脱氢酶。

Defect in signal transduction at the level of the plasma membrane accounts for inability of insulin to activate pyruvate dehydrogenase in white adipocytes of lactating rats.

作者信息

Kilgour E, Vernon R G

机构信息

Hannah Research Institute, Ayr, Scotland, U.K.

出版信息

Biochem J. 1988 Jun 15;252(3):667-72. doi: 10.1042/bj2520667.

Abstract
  1. The mechanism responsible for the failure of insulin to activate pyruvate dehydrogenase (PDH) in white adipose tissue in vivo during lactation was investigated. 2. Insulin failed to increase PDH in isolated adipocytes from lactating rats. 3. Insulin binding to plasma membranes from adipocytes was unchanged by lactation. 4. Incubation of plasma membranes plus permeabilized mitochondria from adipocytes in the presence of insulin resulted in activation of PDH when the plasma membranes were obtained from virgin rats, whereas no activation was observed when plasma membranes from lactating rats were used. 5. The results show that the failure of insulin to activate PDH in adipose tissue from lactating rats is due to a failure of the signal-transduction system in the plasma membrane at steps subsequent to insulin binding to the insulin receptor.
摘要
  1. 研究了哺乳期体内白色脂肪组织中胰岛素未能激活丙酮酸脱氢酶(PDH)的机制。2. 胰岛素未能增加来自哺乳期大鼠的分离脂肪细胞中的PDH。3. 哺乳期对脂肪细胞膜上胰岛素的结合没有影响。4. 当存在胰岛素时,将脂肪细胞膜与透化的线粒体一起孵育,若细胞膜取自未生育大鼠,则会导致PDH激活,而使用哺乳期大鼠的细胞膜时未观察到激活现象。5. 结果表明,哺乳期大鼠脂肪组织中胰岛素未能激活PDH是由于胰岛素与胰岛素受体结合后,质膜信号转导系统在后续步骤中出现故障。

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Intracellular mediators of insulin action.胰岛素作用的细胞内介质。
Vitam Horm. 1984;41:51-78. doi: 10.1016/s0083-6729(08)60087-4.
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Control of fatty acid synthesis in lactation.哺乳期脂肪酸合成的调控
Proc Nutr Soc. 1983 Jun;42(2):315-31. doi: 10.1079/pns19830035.

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