Glutamine synthetase desensitizes differentiated adipocytes to proinflammatory stimuli by raising intracellular glutamine levels

被引：29

作者：

Palmieri, Erika Mariana ^{[1
]}

Spera, Iolanda ^{[1
]}

Menga, Alessio ^{[1
]}

Infantino, Vittoria ^{[2
]}

Iacobazzi, Vito ^{[1
,3
]}

Castegna, Alessandra ^{[1
]}

机构：

[1] Univ Bari, Dept Biosci Biotechnol & Biopharmaceut, I-70125 Bari, Italy

[2] Univ Basilicata, Dept Sci, I-85100 Potenza, Italy

[3] CNR, Inst Biomembranes & Bioenerget, I-70126 Bari, Italy

来源：

FEBS LETTERS | 2014年 / 588卷 / 24期

关键词：

Glutamine; Glutamine synthetase; Adipocyte; Inflammation; Metabolic syndrome; NECROSIS-FACTOR-ALPHA; INTESTINAL EPITHELIAL-CELLS; FACTOR-KAPPA-B; PREADIPOCYTE DIFFERENTIATION; ADIPOSE-TISSUE; CYTOKINE PRODUCTION; INSULIN; GENE; IDENTIFICATION; EXPRESSION;

D O I：

10.1016/j.febslet.2014.11.015

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The role of glutamine synthetase (GS) during adipocyte differentiation is unclear. Here, we assess the impact of GS on the adipocytic response to a proinflammatory challenge at different differentiation stages. GS expression at the late stages of differentiation desensitized mature adipocytes to bacterial lipopolysaccharide (LPS) by increasing intracellular glutamine levels. Furthermore, LPS-activated mature adipocytes were unable to produce inflammatory mediators; LPS sensitivity was rescued following GS inhibition and the associated drop in intracellular glutamine levels. The ability of adipocytes to differentially respond to LPS during differentiation negatively correlates to GS expression and intracellular glutamine levels. Hence, modulation of intracellular glutamine levels by GS expression represents an endogenous mechanism through which mature adipocytes control the inflammatory response. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：4807 / 4814

页数：8

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