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Gene expression profiles of white adipose tissues from C57BL/6 mice in the effect of high fat diet

ABSTRACT: Metabolic disorders including obesity and insulin resistance have their basis in dysregulated lipid metabolism and low-grade inflammation. In a microarray search of unique lipase-related genes whose expressions are associated with obesity, we found that two secreted phospholipase A2s (sPLA2s), PLA2G5 and PLA2G2E, were robustly induced in adipocytes of obese mice. Analyses of Pla2g5-/- and Pla2g2e-/- mice revealed distinct and previously unrecognized roles of these sPLA2s in diet-induced obesity. PLA2G5 hydrolyzed phosphatidylcholine in fat-overladen low-density lipoprotein to release unsaturated fatty acids, which prevented palmitate-induced M1 macrophage polarization. As such, PLA2G5 tipped the immune balance toward an M2 state, thereby counteracting adipose tissue inflammation, insulin resistance, hyperlipidemia and obesiy. PLA2G2E altered minor lipoprotein phospholipids, phosphatidylserine and phosphatidylethanolamine, and moderately facilitated lipid accumulation in adipose tissue and liver. Collectively, the identification of metabolic sPLA2s adds this gene family to a growing list of lipolytic enzymes that act as metabolic coordinators.

ORGANISM(S): Mus musculus

PROVIDER: GSE56038 | GEO | 2014/03/20

SECONDARY ACCESSION(S): PRJNA242276

REPOSITORIES: GEO

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Two secreted phospholipase A2 enzymes, PLA2G5 and PLA2G2E, are induced in hypertrophic adipocytes and distinctly regulate obesity

Project description:Metabolic disorders including obesity and insulin resistance have their basis in dysregulated lipid metabolism and low-grade inflammation. In a microarray search of unique lipase-related genes whose expressions are associated with obesity, we found that two secreted phospholipase A2s (sPLA2s), PLA2G5 and PLA2G2E, were robustly induced in adipocytes of obese mice. Analyses of Pla2g5-/- and Pla2g2e-/- mice revealed distinct and previously unrecognized roles of these sPLA2s in diet-induced obesity. PLA2G5 hydrolyzed phosphatidylcholine in fat-overladen low-density lipoprotein to release unsaturated fatty acids, which prevented palmitate-induced M1 macrophage polarization. As such, PLA2G5 tipped the immune balance toward an M2 state, thereby counteracting adipose tissue inflammation, insulin resistance, hyperlipidemia and obesiy. PLA2G2E altered minor lipoprotein phospholipids, phosphatidylserine and phosphatidylethanolamine, and moderately facilitated lipid accumulation in adipose tissue and liver. Collectively, the identification of metabolic sPLA2s adds this gene family to a growing list of lipolytic enzymes that act as metabolic coordinators. white adipose tissues of C57BL/6 mice; two-condition experimentM-bM-^@M-^Shigh fat diet or low fat diet feeding for 18 weeks; 2 replicates, respectively

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Gene expression analysis of subcutaneous and omental adipose tissue from obese, insulin-resistant women

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Transcriptional co-factor TBLR1 controls lipid mobilization in white adipose tissue

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