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进食与肥胖对人脂肪组织中脂蛋白脂肪酶活性、免疫反应性蛋白及信使核糖核酸水平的影响。

Effect of feeding and obesity on lipoprotein lipase activity, immunoreactive protein, and messenger RNA levels in human adipose tissue.

作者信息

Ong J M, Kern P A

机构信息

Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California 90048.

出版信息

J Clin Invest. 1989 Jul;84(1):305-11. doi: 10.1172/JCI114155.

Abstract

Previous studies have demonstrated higher levels of adipose tissue lipoprotein lipase (LPL) catalytic activity in obese subjects, and in response to a meal. To examine the cellular mechanism of this increase in activity, LPL activity, immunoreactive mass, and mRNA level were measured in lean and obese subjects both before and 4 h after a carbohydrate-rich meal. Heparin-releasable (HR) LPL activity was approximately 2.5-fold higher in the 15 obese subjects, when compared with six lean subjects. However, there was no difference in LPL immunoreactive mass between the lean and obese subjects. In response to the meal, there was a 2.2-fold increase in total adipose tissue LPL activity in the lean subjects due to an increase in both the HR fraction, as well as the adipose fraction extracted with detergents. However, no increase in LPL immunoreactive mass was observed in any adipose tissue LPL fraction, resulting in an increase in LPL specific activity in response to the meal. In the obese subjects, there was no significant increase in LPL activity in response to feeding, and also no increase in immunoreactive mass or specific activity. After extraction of RNA, there was no difference in either the relative proportion of the 3.6- and 3.4-kb human LPL mRNA transcripts, nor in the quantity of LPL mRNA in response to feeding. Thus, these data suggest that the increase in LPL activity under these conditions occurs through a posttranslational activation of a previously inactive LPL precursor.

摘要

先前的研究表明,肥胖受试者以及进食后脂肪组织脂蛋白脂肪酶(LPL)的催化活性水平更高。为了研究这种活性增加的细胞机制,在富含碳水化合物的餐食前后,分别对瘦人和肥胖受试者的LPL活性、免疫反应性物质和mRNA水平进行了测量。与6名瘦人受试者相比,15名肥胖受试者中肝素可释放(HR)LPL活性大约高2.5倍。然而,瘦人和肥胖受试者之间LPL免疫反应性物质并无差异。进食后,瘦人受试者的总脂肪组织LPL活性增加了2.2倍,这是由于HR部分以及用去污剂提取的脂肪部分均增加所致。然而,在任何脂肪组织LPL部分均未观察到LPL免疫反应性物质增加,导致进食后LPL比活性增加。在肥胖受试者中,进食后LPL活性没有显著增加,免疫反应性物质或比活性也没有增加。提取RNA后,3.6 kb和3.4 kb人LPL mRNA转录本的相对比例以及进食后LPL mRNA的数量均无差异。因此,这些数据表明,在这些条件下LPL活性的增加是通过先前无活性的LPL前体的翻译后激活实现的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61cf/303983/d646f6d3dc16/jcinvest00088-0313-a.jpg

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