British Journal of Nutrition

Full Papers

Momordica charantia (bitter melon) reduces plasma apolipoprotein B-100 and increases hepatic insulin receptor substrate and phosphoinositide-3 kinase interactions

Pratibha V. Nerurkara1 c1, Yun Kyung Leea1, Megan Motosuea1, Khosrow Adelia2 and Vivek R. Nerurkara3

a1 Laboratory of Metabolic Disorders and Alternative Medicine, Department of Molecular Biosciences and Bioengineering, College of Tropical Agriculture and Human Resources, University of Hawaii at Manoa, Honolulu, HI 96816, USA

a2 Research Institute, The Hospital for Sick Children, University of Toronto, Toronto, M5G 1X8 Canada

a3 Retrovirology Research Laboratory, Department of Tropical Medicine, Medical Microbiology and Pharmacology, Asia-Pacific Institute of Tropical Medicine and Infectious Diseases, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, HI 96813, USA

Abstract

Aqueous extracts or juice from unripened fruit of Momordica charantia (bitter melon) has traditionally been used in the treatment of diabetes and its complications. Insulin resistance is characterized by significant down-regulation of hepatic insulin signalling as documented by attenuated phosphorylation of insulin receptor (IR), IR substrates 1 and 2, phosphoinositide-3 kinase, protein kinase B, and over-expression of phosphotyrosine phosphatase 1B. We recently demonstrated that bitter melon juice (BMJ) is a potent inhibitor of apoB secretion and TAG synthesis and secretion in human hepatoma cells, HepG2, that may be involved in plasma lipid- and VLDL-lowering effects observed in animal studies. The aim of this study was to evaluate the effects of BMJ on plasma apoB levels and hepatic insulin signalling cascade in mice fed high-fat diet (HFD). Female C57BL/6 mice (4–6 weeks old) were randomized into three groups receiving regular rodent chow, HFD and HFD+BMJ. The data indicate that BMJ not only improves glucose and insulin tolerance but also lowers plasma apoB-100 and apoB-48 in HFD-fed mice as well as modulates the phosphorylation status of IR and its downstream signalling molecules. Investigating the biochemical and molecular mechanisms involved in amelioration of diabetic dyslipidaemia by BMJ may lead to identification of new molecular targets for dietary/alternative therapies.

(Received July 24 2007)

(Revised January 18 2008)

(Accepted January 21 2008)

(Online publication March 05 2008)

Correspondence:

c1 Corresponding author: Dr Pratibha V. Nerurkar, fax +1 808 956 3582, email pratibha@hawaii.edu

Footnotes

Abbreviations: Akt, protein kinase B; BM, bitter melon; BMJ, BM juice; HFD, high-fat diet; IR, insulin receptor; IRS-1, IR substrate 1; IRS-2, IR substrate 2; PI3K, phosphoinositide-3 kinase; PKB, protein kinase B; pTyr, tyrosine phosphorylation status

0Comments