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脂联素通过增加极低密度脂蛋白（VLDL）甘油三酯的分解代谢来降低血浆甘油三酯水平。

Adiponectin reduces plasma triglyceride by increasing VLDL triglyceride catabolism.

作者信息

Qiao Liping, Zou Chenhui, van der Westhuyzen Deneys R, Shao Jianhua

机构信息

Graduate Center for Nutritional Sciences, University of Kentucky, Lexington, Kentucky, USA.

出版信息

Diabetes. 2008 Jul;57(7):1824-33. doi: 10.2337/db07-0435. Epub 2008 Mar 28.

DOI:10.2337/db07-0435
PMID:18375436
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2453618/
Abstract

OBJECTIVE

Adiponectin is an adipocyte-derived hormone that plays an important role in glucose and lipid metabolism. The main aims of this study are to investigate the effects of adiponectin on VLDL triglyceride (VLDL-TG) metabolism and the underlying mechanism.

RESEARCH DESIGN AND METHODS

Adenoviruses were used to generate a mouse model with elevated circulating adiponectin. HepG2 and C2C12 cells were treated with recombinant human adiponectin.

RESULTS

Three days after Ad-mACRP30 adenovirus injection, plasma adiponectin protein levels were increased 12-fold. All three main multimeric adiponectin molecules were proportionally elevated. Fasting plasma TG levels were significantly decreased (approximately 40%) in the mice with elevated adiponectin in circulation, as were the plasma levels of large and medium VLDL subclasses. Although apolipoprotein B mRNA levels were robustly suppressed in the livers of adiponectin-overexpressing mice and in cultured HepG2 cells treated with recombinant human adiponectin, hepatic VLDL-TG secretion rates were not altered by elevated plasma adiponectin. However, Ad-mACRP30-treated mice exhibited a significant increase of postheparin plasma lipoprotein lipase (LPL) activity compared with mice that received control viral vector. Skeletal muscle LPL activity and mRNA levels of LPL and VLDL receptor (VLDLr) were also increased in Ad-mACRP30-treated mice. Recombinant human adiponectin treatment increased LPL and VLDLr mRNA levels in differentiated C1C12 myotubes.

CONCLUSIONS

These results suggest that adiponectin decreases plasma TG levels by increasing skeletal muscle LPL and VLDLr expression and consequently VLDL-TG catabolism.

摘要

目的

脂联素是一种由脂肪细胞分泌的激素，在葡萄糖和脂质代谢中起重要作用。本研究的主要目的是探讨脂联素对极低密度脂蛋白甘油三酯（VLDL-TG）代谢的影响及其潜在机制。

研究设计与方法

使用腺病毒构建循环脂联素水平升高的小鼠模型。用重组人脂联素处理HepG2和C2C12细胞。

结果

注射Ad-mACRP30腺病毒三天后，血浆脂联素蛋白水平增加了12倍。所有三种主要的多聚体脂联素分子均成比例升高。循环中脂联素升高的小鼠空腹血浆甘油三酯水平显著降低（约40%），大、中密度VLDL亚类的血浆水平也降低。尽管在脂联素过表达小鼠的肝脏和用重组人脂联素处理的培养HepG2细胞中载脂蛋白B mRNA水平受到强烈抑制，但血浆脂联素升高并未改变肝脏VLDL-TG的分泌率。然而，与接受对照病毒载体的小鼠相比，Ad-mACRP30处理的小鼠肝素后血浆脂蛋白脂肪酶（LPL）活性显著增加。Ad-mACRP30处理的小鼠骨骼肌LPL活性以及LPL和极低密度脂蛋白受体（VLDLr）的mRNA水平也增加。重组人脂联素处理增加了分化的C1C12肌管中LPL和VLDLr的mRNA水平。

结论

这些结果表明，脂联素通过增加骨骼肌LPL和VLDLr的表达，从而促进VLDL-TG的分解代谢，降低血浆甘油三酯水平。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b79/2453618/60bc03a857da/zdb0070853460007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b79/2453618/13b774b1ff6d/zdb0070853460001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b79/2453618/5f9ca587f860/zdb0070853460002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b79/2453618/4f11e780bb73/zdb0070853460003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b79/2453618/739e95498fa5/zdb0070853460004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b79/2453618/a3d402421c37/zdb0070853460005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b79/2453618/098d644072b4/zdb0070853460006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b79/2453618/60bc03a857da/zdb0070853460007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b79/2453618/13b774b1ff6d/zdb0070853460001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b79/2453618/5f9ca587f860/zdb0070853460002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b79/2453618/4f11e780bb73/zdb0070853460003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b79/2453618/739e95498fa5/zdb0070853460004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b79/2453618/a3d402421c37/zdb0070853460005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b79/2453618/098d644072b4/zdb0070853460006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b79/2453618/60bc03a857da/zdb0070853460007.jpg

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