title: Momordica charantia (Bitter Melon) reduces obesity-associated macrophage and mast cell infiltration as well as inflammatory cytokine expression in adipose tissues.
abstract: Obesity is a world-wide epidemic disease that correlates closely with type 2 diabetes and cardiovascular diseases. Obesity-induced chronic adipose tissue inflammation is now considered as a critical contributor to the above complications. Momordica charantia (bitter melon, BM) is a traditional Chinese food and well known for its function of reducing body weight gain and insulin resistance. However, it is unclear whether BM could alleviate adipose tissue inflammation caused by obesity. In this study, C57BL/6 mice were fed high fat diet (HFD) with or without BM for 12 weeks. BM-contained diets ameliorated HFD-induced obesity and insulin resistance. Histological and real-time PCR analysis demonstrated BM not only reduced macrophage infiltration into epididymal adipose tissues (EAT) and brown adipose tissues (BAT). Flow cytometry show that BM could modify the M1/M2 phenotype ratio of macrophages in EAT. Further study showed that BM lowered mast cell recruitments in EAT, and depressed pro-inflammatory cytokine monocyte chemotactic protein-1 (MCP-1) expression in EAT and BAT as well as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) expression in EAT. Finally, ELISA analysis showed BM-contained diets also normalized serum levels of the cytokines. In summary, in concert with ameliorated insulin resistance and fat deposition, BM reduced adipose tissue inflammation in diet-induced obese (DIO) mice.
authors.affiliation: School of Biotechnology and Food Engineering, Hefei University of Technology, Hefei, China.
authors.forename: Bin
authors.initials: B
authors.lastname: Bao
authors.affiliation: School of Biotechnology and Food Engineering, Hefei University of Technology, Hefei, China.
authors.forename: Yan-Guang
authors.initials: YG
authors.lastname: Chen
authors.affiliation: School of Biotechnology and Food Engineering, Hefei University of Technology, Hefei, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Zhang
authors.affiliation: School of Biotechnology and Food Engineering, Hefei University of Technology, Hefei, China.
authors.forename: Yan Lin
authors.initials: YL
authors.lastname: Na Xu
authors.affiliation: School of Biotechnology and Food Engineering, Hefei University of Technology, Hefei, China.
authors.forename: Xin
authors.initials: X
authors.lastname: Wang
authors.affiliation: School of Biotechnology and Food Engineering, Hefei University of Technology, Hefei, China.
authors.forename: Jian
authors.initials: J
authors.lastname: Liu
authors.affiliation: School of Biotechnology and Food Engineering, Hefei University of Technology, Hefei, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Qu
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism* / Q000473:pathology*; D050154:Adiposity; D000818:Animals; D016207:Cytokines / Q000097:blood / Q000378:metabolism; D004032:Diet; D018836:Inflammation Mediators / Q000097:blood / Q000378:metabolism; D007333:Insulin Resistance; D008264:Macrophages / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008407:Mast Cells / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D029777:Momordica charantia / Q000737:chemistry*; D009765:Obesity / Q000178:diet therapy / Q000209:etiology / Q000378:metabolism*; D010641:Phenotype
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators