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脂肪组织单酰甘油脂肪酶 1 在小鼠和人类中的代谢重要性。

Metabolic importance of adipose tissue monoacylglycerol acyltransferase 1 in mice and humans.

机构信息

Department of Pediatrics Washington University School of Medicine, St. Louis, MO 63110.

Medicine, Washington University School of Medicine, St. Louis, MO 63110.

出版信息

J Lipid Res. 2018 Sep;59(9):1630-1639. doi: 10.1194/jlr.M084947. Epub 2018 May 31.

DOI:10.1194/jlr.M084947
PMID:29853530
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6121930/
Abstract

Adipocyte triglyceride storage provides a reservoir of energy that allows the organism to survive times of nutrient scarcity, but excessive adiposity has emerged as a health problem in many areas of the world. Monoacylglycerol acyltransferase (MGAT) acylates monoacylglycerol to produce diacylglycerol; the penultimate step in triglyceride synthesis. However, little is known about MGAT activity in adipocytes, which are believed to rely primarily on another pathway for triglyceride synthesis. We show that expression of the gene that encodes MGAT1 is robustly induced during adipocyte differentiation and that its expression is suppressed in fat of genetically-obese mice and metabolically-abnormal obese human subjects. Interestingly, MGAT1 expression is also reduced in physiologic contexts where lipolysis is high. Moreover, knockdown or knockout of MGAT1 in adipocytes leads to higher rates of basal adipocyte lipolysis. Collectively, these data suggest that MGAT1 activity may play a role in regulating basal adipocyte FFA retention.

摘要

脂肪细胞甘油三酯储存提供了能量储备,使机体能够在营养匮乏时存活,但在世界许多地区,过多的肥胖已成为一个健康问题。单酰基甘油脂肪酶(MGAT)将单酰甘油酰化为二酰甘油,这是甘油三酯合成的倒数第二步。然而,人们对脂肪细胞中的 MGAT 活性知之甚少,据信脂肪细胞主要依赖另一种途径合成甘油三酯。我们发现,编码 MGAT1 的基因的表达在脂肪细胞分化过程中被强烈诱导,并且在肥胖基因小鼠和代谢异常肥胖的人类受试者的脂肪中其表达受到抑制。有趣的是,MGAT1 的表达在脂肪分解率高的生理环境中也会降低。此外,脂肪细胞中 MGAT1 的敲低或敲除导致基础脂肪细胞脂肪分解率升高。总的来说,这些数据表明 MGAT1 活性可能在调节基础脂肪细胞游离脂肪酸保留中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5eb4/6121930/844a9089b275/1630fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5eb4/6121930/a34cbafbefa0/1630fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5eb4/6121930/54d14c528770/1630fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5eb4/6121930/e41b498c30cb/1630fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5eb4/6121930/00c6aa86eb48/1630fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5eb4/6121930/48c399faa085/1630fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5eb4/6121930/8be965b913a8/1630fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5eb4/6121930/844a9089b275/1630fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5eb4/6121930/a34cbafbefa0/1630fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5eb4/6121930/54d14c528770/1630fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5eb4/6121930/e41b498c30cb/1630fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5eb4/6121930/00c6aa86eb48/1630fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5eb4/6121930/48c399faa085/1630fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5eb4/6121930/8be965b913a8/1630fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5eb4/6121930/844a9089b275/1630fig7.jpg

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