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去营养蛋白在脂肪组织中的过表达促进脂肪酸利用并减轻饮食诱导的肥胖。

Adipose overexpression of desnutrin promotes fatty acid use and attenuates diet-induced obesity.

作者信息

Ahmadian Maryam, Duncan Robin E, Varady Krista A, Frasson Danubia, Hellerstein Marc K, Birkenfeld Andreas L, Samuel Varman T, Shulman Gerald I, Wang Yuhui, Kang Chulho, Sul Hei Sook

机构信息

Department of Nutritional Science and Toxicology, University of California, Berkeley, California, USA.

出版信息

Diabetes. 2009 Apr;58(4):855-66. doi: 10.2337/db08-1644. Epub 2009 Jan 9.

DOI:10.2337/db08-1644
PMID:19136649
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2661591/
Abstract

OBJECTIVE

To investigate the role of desnutrin in adipose tissue triacylglycerol (TAG) and fatty acid metabolism.

RESEARCH DESIGN AND METHODS

We generated transgenic mice overexpressing desnutrin (also called adipose triglyceride lipase [ATGL]) in adipocytes (aP2-desnutrin) and also performed adenoviral-mediated overexpression of desnutrin in 3T3-L1CARDelta1 adipocytes.

RESULTS

aP2-desnutrin mice were leaner with decreased adipose tissue TAG content and smaller adipocyte size. Overexpression of desnutrin increased lipolysis but did not result in increased serum nonesterified fatty acid levels or ectopic TAG storage. We found increased cycling between diacylglycerol (DAG) and TAG and increased fatty acid oxidation in adipocytes from these mice, as well as improved insulin sensitivity.

CONCLUSIONS

We show that by increasing lipolysis, desnutrin overexpression causes reduced adipocyte TAG content and attenuation of diet-induced obesity. Desnutrin-mediated lipolysis promotes fatty acid oxidation and re-esterification within adipocytes.

摘要

目的

研究去营养蛋白在脂肪组织甘油三酯（TAG）和脂肪酸代谢中的作用。

研究设计与方法

我们构建了在脂肪细胞中过表达去营养蛋白（也称为脂肪甘油三酯脂肪酶[ATGL]）的转基因小鼠（aP2-去营养蛋白），并在3T3-L1CARDelta1脂肪细胞中进行了腺病毒介导的去营养蛋白过表达。

结果

aP2-去营养蛋白小鼠体型更瘦，脂肪组织TAG含量降低，脂肪细胞尺寸更小。去营养蛋白的过表达增加了脂肪分解，但并未导致血清非酯化脂肪酸水平升高或异位TAG储存增加。我们发现这些小鼠脂肪细胞中甘油二酯（DAG）和TAG之间的循环增加，脂肪酸氧化增加，胰岛素敏感性也得到改善。

结论

我们表明，通过增加脂肪分解，去营养蛋白过表达导致脂肪细胞TAG含量降低和饮食诱导的肥胖减轻。去营养蛋白介导的脂肪分解促进脂肪细胞内的脂肪酸氧化和再酯化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f26/2661591/c16a45659d2d/zdb0040956830008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f26/2661591/4ebd72f4eddc/zdb0040956830001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f26/2661591/24903a32a6c7/zdb0040956830002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f26/2661591/b856936050c3/zdb0040956830003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f26/2661591/f0cdb9724260/zdb0040956830004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f26/2661591/6a8861a45838/zdb0040956830005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f26/2661591/9b29fbcded4d/zdb0040956830006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f26/2661591/0667b147a937/zdb0040956830007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f26/2661591/c16a45659d2d/zdb0040956830008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f26/2661591/4ebd72f4eddc/zdb0040956830001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f26/2661591/24903a32a6c7/zdb0040956830002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f26/2661591/b856936050c3/zdb0040956830003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f26/2661591/f0cdb9724260/zdb0040956830004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f26/2661591/6a8861a45838/zdb0040956830005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f26/2661591/9b29fbcded4d/zdb0040956830006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f26/2661591/0667b147a937/zdb0040956830007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f26/2661591/c16a45659d2d/zdb0040956830008.jpg

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