Bitter gourd inhibits the development of obesity-associated fatty liver in C57BL/6 mice fed a high-fat diet

J Nutr. 2014 Apr;144(4):475-83. doi: 10.3945/jn.113.187450. Epub 2014 Feb 12.


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.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Biomarkers / blood
  • Biomarkers / metabolism
  • China
  • Diet, High-Fat / adverse effects*
  • Dietary Supplements*
  • Fatty Liver / etiology
  • Fatty Liver / prevention & control*
  • Freeze Drying
  • Fruit / chemistry*
  • Hyperglycemia / etiology
  • Hyperglycemia / prevention & control
  • Hyperlipidemias / etiology
  • Hyperlipidemias / prevention & control
  • Insulin Resistance
  • Lipotropic Agents / administration & dosage
  • Lipotropic Agents / therapeutic use*
  • Liver / immunology
  • Liver / metabolism
  • Liver / pathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mitochondria, Liver / enzymology
  • Mitochondria, Liver / metabolism
  • Mitochondria, Liver / pathology
  • Momordica charantia / chemistry*
  • Non-alcoholic Fatty Liver Disease
  • Obesity / etiology
  • Obesity / immunology
  • Obesity / metabolism
  • Obesity / physiopathology*
  • Oxidative Stress
  • Random Allocation


  • Biomarkers
  • Lipotropic Agents