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

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 eleva...

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Veröffentlicht in:	Diabetes (New York, N.Y.) N.Y.), 2019-06, Vol.68 (6), p.1130-1142
Hauptverfasser:	Chen, Xiaofang, Zhuo, Shu, Zhu, Tengfei, Yao, Pengle, Yang, Mengmei, Mei, Hong, Li, Na, Ma, Fengguang, Wang, Ji Ming, Chen, Shiting, Ye, Richard D, Li, Yu, Le, Yingying
Format:	Artikel
Sprache:	eng
Schlagworte:	Adipocytes Adipose tissue Amyloid Animals Body fat Body temperature Body Temperature - genetics Body weight gain Bone marrow transplantation Chemotaxis Chemotaxis - genetics Clonal deletion Diet, High-Fat Energy expenditure Energy Metabolism - genetics Fatty liver Fatty Liver - genetics Fatty Liver - immunology Glucose High fat diet Hyperglycemia Hyperglycemia - genetics Hyperglycemia - immunology Hyperlipidemia Hyperlipidemias - genetics Hyperlipidemias - immunology Immune response Inflammation Inflammation - genetics Inflammation - immunology Insulin Insulin resistance Insulin Resistance - genetics Insulin Resistance - immunology Lipopolysaccharides Macrophages Macrophages - immunology Metabolic disorders Metabolism Mice Mice, Knockout Mice, Obese Nutrient deficiency Obesity Palmitic acid Polarization Receptors, Formyl Peptide - genetics Serum Amyloid A Protein - metabolism Skeletal muscle Thermogenesis - genetics γ-Interferon
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