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Fpr2 Deficiency Alleviates Diet-Induced Insulin Resistance Through Reducing Body Weight Gain and Inhibiting Inflammation Mediated by Macrophage Chemotaxis and M1 Polarization

文献类型：期刊论文

作者Chen, Xiaofang1; Zhuo, Shu1; Zhu, Tengfei1; Yao, Pengle1; Yang, Mengmei1; Mei, Hong1; Li, Na1; Ma, Fengguang1; Chen, Shiting1; Li, Yu1
刊名DIABETES
出版日期2019
卷号68期号:6页码:1130-1142
关键词hepatocellular carcinoma patient-derived tumor grafts sorafenib drug resistance
ISSN号0012-1797
DOI10.2337/db18-0469
文献子类Article
英文摘要Obesity and related inflammation are critical for the pathogenesis of insulin resistance, but the underlying mechanisms are not fully understood. Formyl peptide receptor 2 (FPR2) plays important roles in host immune responses and inflammation-related diseases. We found that Fpr2 expression was elevated in the white adipose tissue of high-fat diet (HFD)-induced obese mice and db/db mice. The systemic deletion of Fpr2 alleviated HFD-induced obesity, insulin resistance, hyperglycemia, hyperlipidemia, and hepatic steatosis. Furthermore, Fpr2 deletion in HFD-fed mice elevated body temperature, reduced fat mass, and inhibited inflammation by reducing macrophage infiltration and M1 polarization in metabolic tissues. Bone marrow transplantations between wild-type and Fpr2(-/-) mice and myeloid-specific Fpr2 deletion demonstrated that Fpr2-expressing myeloid cells exacerbated HFD-induced obesity, insulin resistance, glucose/lipid metabolic disturbances, and inflammation. Mechanistic studies revealed that Fpr2 deletion in HFD-fed mice enhanced energy expenditure probably through increasing thermogenesis in skeletal muscle; serum amyloid A3 and other factors secreted by adipocytes induced macrophage chemotaxis via Fpr2; and Fpr2 deletion suppressed macrophage chemotaxis and lipopolysaccharide-, palmitate-, and interferon-gamma-induced macrophage M1 polarization through blocking their signals. Altogether, our studies demonstrate that myeloid Fpr2 plays critical roles in obesity and related metabolic disorders via regulating muscle energy expenditure, macrophage chemotaxis, and M1 polarization.
学科主题Endocrinology & Metabolism
WOS关键词SERUM AMYLOID A3 ; FORMYL PEPTIDE RECEPTORS ; FAT ; ADIPOCYTES ; EXPRESSION ; MECHANISM ; OBESITY ; THERMOGENESIS ; RESPONSES ; KINASE
语种英语
WOS记录号WOS:000468311600004
出版者AMER DIABETES ASSOC
版本出版稿
源URL[http://202.127.25.144/handle/331004/579]  
专题中国科学院上海生命科学研究院营养科学研究所
作者单位1.Chinese Acad Sci, Univ Chinese Acad Sci, Shanghai Inst Biol Sci, CAS Key Lab Nutr Metab & Food Safety,Shanghai Ins, Shanghai, Peoples R China;
2.Minist Hlth, Key Lab Food Safety Risk Assessment, Beijing, Peoples R China,
3.Univ Macau, Inst Chinese Med Sci, Taipa, Macau, Peoples R China;
4.NCI, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21701 USA;
推荐引用方式
GB/T 7714		 Chen, Xiaofang,Zhuo, Shu,Zhu, Tengfei,et al. Fpr2 Deficiency Alleviates Diet-Induced Insulin Resistance Through Reducing Body Weight Gain and Inhibiting Inflammation Mediated by Macrophage Chemotaxis and M1 Polarization[J]. DIABETES,2019,68(6):1130-1142.
APA Chen, Xiaofang.,Zhuo, Shu.,Zhu, Tengfei.,Yao, Pengle.,Yang, Mengmei.,...&,.(2019).Fpr2 Deficiency Alleviates Diet-Induced Insulin Resistance Through Reducing Body Weight Gain and Inhibiting Inflammation Mediated by Macrophage Chemotaxis and M1 Polarization.DIABETES,68(6),1130-1142.
MLA Chen, Xiaofang,et al."Fpr2 Deficiency Alleviates Diet-Induced Insulin Resistance Through Reducing Body Weight Gain and Inhibiting Inflammation Mediated by Macrophage Chemotaxis and M1 Polarization".DIABETES 68.6(2019):1130-1142.

入库方式： OAI收割

来源：上海营养与健康研究所

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