Abstract

Momordica charantia (bitter melon, BM) has traditionally been used in the treatment of diabetes and its complications. Insulin resistance is characterized by resistance to insulin‐stimulated glucose uptake, leading to enhanced very low density lipoprotein (VLDL) secretion, and significant down‐regulation of hepatic insulin signaling as documented by attenuated phosphorylation of i54 nsulin receptor (IR), IR substrates (IRS‐1/IRS‐2) and PI3K, PKB/Akt. Our recent studies demonstrated that BM juice (BMJ) can significantly reduce apoB secretion, in human hepatoma cells, HepG2. The aim of our study was to evaluate the effects of BMJ on plasma apoB levels and hepatic insulin signaling cascade in mice fed high fat diet (HFD). Four to six weeks old female C57BL/6 mice were randomized into three groups of control, receiving regular rodent chow with 11 kcal% fat; high fat diet (HFD), receiving chow containing 58 kcal% fat; and HDF + 1.5% lyophilized BMJ. Our data indicates that BMJ lowers plasma apoB‐100 and apoB‐48 in HFD‐fed mice by improving the phosphorylation status of insulin receptor and its downstream signaling molecules. Investigating the mechanisms mediated by BMJ to ameliorate diabetic dyslipidemia may lead to identification of new molecular targets for dietary therapies. [Grant support by RCMI, NIH/NCRR, G12RR00361; Hawaii Community Foundation, 20041652 and NIH/NCCAM 1R21AT003719‐01A1].

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