| Literature DB >> 24910243 |
Hiroyasu Sato1, Yoshitaka Taketomi1, Ayako Ushida2, Yuki Isogai2, Takumi Kojima3, Tetsuya Hirabayashi3, Yoshimi Miki1, Kei Yamamoto3, Yasumasa Nishito4, Tetsuyuki Kobayashi5, Kazutaka Ikeda6, Ryo Taguchi7, Shuntaro Hara8, Satoshi Ida9, Yuji Miyamoto9, Masayuki Watanabe9, Hideo Baba9, Keishi Miyata10, Yuichi Oike10, Michael H Gelb11, Makoto Murakami12.
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 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 obesity. 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.Entities:
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Year: 2014 PMID： 24910243 PMCID： PMC4079757 DOI： 10.1016/j.cmet.2014.05.002
Source DB: PubMed Journal: Cell Metab ISSN： 1550-4131 Impact factor: 27.287