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生长激素降低脂肪组织生长的机制。

Mechanisms by which somatotropin decreases adipose tissue growth.

作者信息

Etherton T D, Louveau I, Sørensen M T, Chaudhuri S

机构信息

Department of Dairy and Animal Science, Pennsylvania State University, University Park 16802.

出版信息

Am J Clin Nutr. 1993 Aug;58(2 Suppl):287S-295S. doi: 10.1093/ajcn/58.2.287S.

Abstract

When growing pigs are treated daily with recombinantly derived porcine somatotropin (pST) for 30-60 d there is a dose-dependent decrease in lipid accretion. Maximal doses of pST can reduce lipid accretion by as much as 70%. The reduction in lipid accretion occurs because of a marked decrease in glucose transport and lipogenesis that is the result of a pST-dependent decrease in the ability of insulin to stimulate these processes in the adipocyte; lipolysis is not affected. The decrease in insulin sensitivity is not due to a decrease in insulin binding or insulin receptor kinase activity. Little is understood about the somatotropin (ST) intracellular signal pathway(s) that mediate the biological effects of ST. These effects are chronic rather than acute as was previously believed. This pattern likely reflects that ST decreases transcription of important insulin-responsive genes such as the muscle-adipose tissue transporter gene (GLUT4) and key lipogenic enzymes.

摘要

对生长猪每日注射重组猪生长激素(pST)30至60天,会出现脂质蓄积的剂量依赖性降低。最大剂量的pST可使脂质蓄积减少多达70%。脂质蓄积减少是因为葡萄糖转运和脂肪生成显著减少,这是由于pST依赖的胰岛素刺激脂肪细胞中这些过程的能力下降所致;脂肪分解不受影响。胰岛素敏感性降低并非由于胰岛素结合或胰岛素受体激酶活性下降。对于介导生长激素(ST)生物学效应的细胞内信号通路知之甚少。这些效应是慢性的,而非如先前认为的是急性的。这种模式可能反映出ST降低了重要的胰岛素反应基因的转录,如肌肉 - 脂肪组织转运蛋白基因(GLUT4)和关键的脂肪生成酶。

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