期刊
CELL METABOLISM
卷 20, 期 1, 页码 119-132出版社
CELL PRESS
DOI: 10.1016/j.cmet.2014.05.002
关键词
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资金
- Ministry of Education, Culture, Sports, Science and Technology of Japan [22116005, 24390021, 23790120, 25860059, 24117724, 23790119]
- CREST from the Japan Science and Technology Agency
- Uehara Foundation
- Mitsubishi Foundation
- Terumo Foundation
- Toray Science Foundation
- National Institutes of Health [HL36235]
- Grants-in-Aid for Scientific Research [25860059, 22116001, 24117724, 22116005, 23790120, 25504004, 24390021, 25460087, 26461671, 25116720, 24619007, 23790119] Funding Source: KAKEN
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 A(2)s (sPLA(2)s), PLA2G5 and PLA2G2E, were robustly induced in adipocytes of obese mice. Analyses of Pla2g5(-/-) and Pla2g2e(-/-) mice revealed distinct roles of these sPLA(2)s 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.
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