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首页> 外文期刊>Cell metabolism >The adipocyte-inducible secreted phospholipases PLA2G5 and PLA2G2E play distinct roles in obesity
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The adipocyte-inducible secreted phospholipases PLA2G5 and PLA2G2E play distinct roles in obesity

机译：脂肪细胞诱导的分泌型磷脂酶PLA2G5和PLA2G2E在肥胖中起不同的作用

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摘要

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.
机译：包括肥胖和胰岛素抵抗在内的代谢紊乱是脂质代谢失调和低度炎症的基础。在其表达与肥胖相关的独特的脂肪酶相关基因的微阵列搜索中，我们发现肥胖小鼠的脂肪细胞中强烈诱导了两种分泌的磷脂酶A2（sPLA2s）PLA2G5和PLA2G2E。对Pla2g5-/-和Pla2g2e-//-小鼠的分析显示，这些sPLA2在饮食诱导的肥胖中具有不同的作用。 PLA2G5水解覆脂的低密度脂蛋白中的磷脂酰胆碱以释放不饱和脂肪酸，从而阻止了棕榈酸酯诱导的M1巨噬细胞极化。这样，PLA2G5使免疫平衡趋于M2状态，从而抵消了脂肪组织炎症，胰岛素抵抗，高脂血症和肥胖症。 PLA2G2E改变了次要脂蛋白磷脂，磷脂酰丝氨酸和磷脂酰乙醇胺，并适度促进了脂肪在脂肪组织和肝脏中的蓄积。总的来说，“代谢性sPLA2s”的鉴定将这个基因家族添加到了越来越多的充当代谢协调剂的脂解酶中。

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