title: Bitter gourd inhibits the development of obesity-associated fatty liver in C57BL/6 mice fed a high-fat diet.
abstract: Bitter gourd (BG) is a popular fruit in Asia with numerous well-known medicinal uses, including as an antidiabetic. In the current study, we aimed to explore the effects of BG on mitochondrial function during the development of obesity-associated fatty liver. C57BL/6 mice were divided into 4 experimental groups: mice fed a normal diet (control; included for reference only), mice fed a high-fat diet (HFD), and mice fed an HFD supplemented with freeze-dried BG powder through daily gavage at doses of 0.5 (HFD+0.5BG) and 5 (HFD+5BG) g/kg, respectively. After 16 wk, mice in the HFD+5BG group showed less body and tissue weight gain and less hyperglycemia and hyperlipidemia compared with those in the HFD group (P < 0.05). In both HFD+0.5BG and HFD+5BG groups, serum interleukin-6 concentration was lower than that in the HFD group (P < 0.02). The serum C-reactive protein concentration was lower in the HFD+5BG group compared with the HFD group (P < 0.04). An analysis of liver tissue revealed lower liver triglyceride and cholesterol concentrations in both HFD+0.5BG and HFD+5BG groups than in the HFD group (P < 0.01). The HFD+5BG group had less activation of the sterol regulatory element binding protein/fatty acid synthase (SREBP-1/FAS) pathway, greater superoxide dismutase activity, and less total protein and mitochondrial protein oxidation than did the HFD group (P < 0.05). Mitochondrial complex I, II, III, and V activity was greater in the HFD+0.5BG group than in the HFD group (P < 0.03). The HFD+5BG group only had greater complex V activity compared with the HFD group (P < 0.05). Mitochondrial dynamics regulators, including dynamin related protein 1 (DRP1) and mitofusin 1 (MFN1), as well as proapoptotic protein expression levels were restored by BG treatment (P < 0.02). Taken together, our results suggest that BG prevents inflammation and oxidative stress, modulates mitochondrial activity, suppresses apoptosis activation, and inhibits lipid accumulation during the development of fatty liver.
authors: Centers for Mitochondrial Biology & Medicine and.
authors: Jie
authors: J
authors: Xu
authors: Ke
authors: K
authors: Cao
authors: Yuan
authors: Y
authors: Li
authors: Xuan
authors: X
authors: Zou
authors: Cong
authors: C
authors: Chen
authors: Ignatius Man-Yau
authors: IM
authors: Szeto
authors: Zhizhong
authors: Z
authors: Dong
authors: Youyou
authors: Y
authors: Zhao
authors: Yujie
authors: Y
authors: Shi
authors: Junkuan
authors: J
authors: Wang
authors: Jiankang
authors: J
authors: Liu
authors: Zhihui
authors: Z
authors: Feng
mesh_terms: D000818:Animals; D017209:Apoptosis; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D002681:China; D059305:Diet, High-Fat / Q000009:adverse effects*; D019587:Dietary Supplements; D005234:Fatty Liver / Q000209:etiology / Q000517:prevention & control*; D005612:Freeze Drying; D005638:Fruit / Q000737:chemistry*; D006943:Hyperglycemia / Q000209:etiology / Q000517:prevention & control; D006949:Hyperlipidemias / Q000209:etiology / Q000517:prevention & control; D007333:Insulin Resistance; D008082:Lipotropic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D008099:Liver / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008930:Mitochondria, Liver / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D029777:Momordica charantia / Q000737:chemistry*; D065626:Non-alcoholic Fatty Liver Disease; D009765:Obesity / Q000209:etiology / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology*; D018384:Oxidative Stress; D011897:Random Allocation
chemical_list: D015415:Biomarkers; D008082:Lipotropic Agents