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人 LPIN1 基因与皮下和内脏脂肪组织缺氧及内质网应激基因的关系

Relation between human LPIN1, hypoxia and endoplasmic reticulum stress genes in subcutaneous and visceral adipose tissue.

机构信息

Unitat de Recerca, Hospital Universitari de Tarragona Joan XXIII, IISPV, Tarragona, Spain.

出版信息

Int J Obes (Lond). 2010 Apr;34(4):679-86. doi: 10.1038/ijo.2009.290. Epub 2010 Jan 26.

Abstract

CONTEXT

LPIN1 is the phosphatidic acid phosphatase that produces 1,2-diacylglycerol, and thus it is related to the synthesis of triglycerides in the adipocyte. LPIN1 has a role in lipid synthesis and nuclear receptor coactivation, both of which may be involved in lipid homeostasis and metabolism. Among others, hypoxia and endoplasmic reticulum (ER) stress are being shown to be related to the adipose dysfunction found in human obesity.

OBJECTIVE

The aim of this study was to analyze LPIN1 gene expression in human adipose tissue in parallel with several hypoxia, angiogenic, ER stress and peroxisome proliferator-activated receptor (PPAR)-related genes in human obesity.

DESIGN AND PATIENTS

Gene expression was quantified in abdominal (subcutaneous and visceral) adipose tissue from 62 subjects.

RESULTS

We have shown a marked association between LPIN1 and PPARalpha gene expression both in subcutaneous and visceral adipose tissues. Similarly, a strong interdependence with vascular endothelial growth factor (VEGF) gene expression was also described; in fact, LPIN1 and VEGF expression levels were significantly decreased with obesity to a similar extent.

CONCLUSION

These associations might suggest a possible role of LPIN1 in stress conditions that occur in chronic obesity and underlie insulin resistance.

摘要

背景

LPIN1 是产生 1,2-二酰基甘油的磷酸脂酶,因此它与脂肪细胞中甘油三酯的合成有关。LPIN1 在脂质合成和核受体共激活中发挥作用,这两者都可能与脂质稳态和代谢有关。除其他因素外,缺氧和内质网(ER)应激被证明与人类肥胖症中发现的脂肪功能障碍有关。

目的

本研究旨在分析人类肥胖症中 LPIN1 基因在人脂肪组织中的表达,并与几种缺氧、血管生成、ER 应激和过氧化物酶体增殖物激活受体(PPAR)相关基因平行分析。

设计和患者

定量分析了 62 名受试者腹部(皮下和内脏)脂肪组织中的基因表达。

结果

我们已经表明,LPIN1 与 PPARalpha 基因在皮下和内脏脂肪组织中的表达都有明显的关联。同样,也描述了与血管内皮生长因子(VEGF)基因表达的强烈相互依赖性;事实上,LPIN1 和 VEGF 的表达水平随着肥胖程度的增加而显著降低。

结论

这些关联可能表明 LPIN1 在慢性肥胖和胰岛素抵抗下发生的应激条件下可能发挥作用。

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