• Chun-Ching Shih, Cheng-Hsiu Lin, Wei-Li Lin, and Jin-Bin Wu.
• Institute of Pharmaceutical Science and Technology, College of Health Science, Central Taiwan University of Science and Technology, 11, Po-Tze Lane, Takun, Taichung 406, Taiwan, ROC. ccshih@ctust.edu.tw
• J Ethnopharmacol. 2009 May 4; 123 (1): 82-90.

Aim Of The StudyWe investigated the preventive effect of Momordica charantia Linn. (Cucurbitaceae) fruit, commonly known as bitter melon, on hyperglycemia and insulin resistance in rats fed with a fructose-enriched diet.Materials And MethodsFirst, rats were divided randomly into two groups: the control group was fed with control diet, whereas the experimental group was fed with a 60% high-fructose diet for 8 weeks. After the first 6 weeks, the fructose-treated rats were further subdivided into six groups and were orally fed with or without Momordica charantia L. or rosiglitazone (ROS) for 2 weeks while rats were still on fructose diet.ResultsWe demonstrated that bitter melon was effective in ameliorating the fructose diet-induced hyperglycemia, hyperleptinemia, hyperinsulinemia, and hypertriglyceridemia as well as in decreasing the levels of free fatty acid (FFA) (P<0.001, P<0.05, P<0.05, P<0.05, P<0.05, respectively). Bitter melon reversed fructose diet-induced hypoadiponectinemia (P<0.05), which provides a therapeutic advantage to insulin resistance in improving insulin sensitivity. Additionally, bitter melon decreased the weights of epididymal (P<0.05) and retroperitoneal white adipose tissue (WAT) (P<0.05). Bitter melon increased the expression of peroxisome proliferator-activated receptor gamma (PPAR gamma) in white adipose tissue (WAT). Conversely, bitter melon decreased the expression of leptin in WAT. Furthermore, we demonstrate that bitter melon significantly increases the mRNA expression and protein of glucose transporter 4 (GLUT4) in skeletal muscle.ConclusionsThis study demonstrates, for the first time, the beneficial effects of two different extracts of bitter melon on insulin resistance in rats fed a high-fructose diet thereby producing evidence of the role of changes in expression of PPAR gamma and GLUT4.

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