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Food Chem Toxicol. 2014 Jul;69:347-56. doi: 10.1016/j.fct.2014.04.008. Epub 2014 Apr 18.

Differential anti-diabetic effects and mechanism of action of charantin-rich extract of Taiwanese Momordica charantia between type 1 and type 2 diabetic mice.

Author information

1
Division of Nephrology, Chi Mei Medical Center, Yong-Kang District, Tainan City, Taiwan; Department of Sports Management, College of Leisure and Recreation Management, Chia Nan University of Pharmacy and Science, Rende District, Tainan City, Taiwan.
2
Division of Nephrology, Chi Mei Medical Center, Yong-Kang District, Tainan City, Taiwan; Department of Medical Laboratory Science and Biotechnology, Chung Hua University of Medical Technology, Rende District, Tainan City, Taiwan.
3
Department of Neurology, Chi Mei Medical Center, Yong-Kang District, Tainan City, Taiwan; Department of Occupational Medicine, Chi Mei Medical Center, Yong-Kang District, Tainan City, Taiwan; Department of Occupational Safety, College of Environment, Chia Nan University of Pharmacy and Science, Rende District, Tainan City, Taiwan; Department of Occupational and Environmental Medicine, National Cheng Kung University Hospital, North District, Tainan City, Taiwan.
4
Institute of Biotechnology, College of Engineering, Southern Taiwan University of Science and Technology, Yong-Kang District, Tainan City, Taiwan.
5
Institute of Biotechnology, College of Engineering, Southern Taiwan University of Science and Technology, Yong-Kang District, Tainan City, Taiwan. Electronic address: jjchuu@mail.stust.edu.tw.

Abstract

Momordica charantia Linn. (Cucurbitaceae), also called bitter melon, has traditionally been used as a natural anti-diabetic agent for anti-hyperglycemic activity in several animal models and clinical trials. We investigated the differences in the anti-diabetic properties and mechanism of action of Taiwanese M. charantia (MC) between type 1 diabetic (T1D) and type 2 diabetic (T2D) mice. To clarify the beneficial effects of MC, we measured non-fasting glucose, oral glucose tolerance, and plasma insulin levels in KK/HIJ mice with high-fat diet-induced diabetes (200 mg/kg/day of charantin-rich extract of MC [CEMC]) and in ICR mice with STZ-induced diabetes. After 8 weeks, all the mice were exsanguinated, and the expression of the insulin-signaling-associated proteins in their tissue was evaluated, in coordination with the protective effects of CEMC against pancreatic β-cell toxicity (in vitro). Eight weeks of data indicated that CEMC caused a significant decline in non-fasting blood glucose, plasma glucose intolerance, and insulin resistance in the KK/HIJ mice, but not in the ICR mice. Furthermore, CEMC decreased plasma insulin and promoted the sensitivity of insulin by increasing the expression of GLUT4 in the skeletal muscle and of IRS-1 in the liver of KK/HIJ mice; however, CEMC extract had no effect on the insulin sensitivity of ICR mice. In vitro study showed that CEMC prevented pancreatic β cells from high-glucose-induced cytotoxicity after 24 h of incubation, but the protective effect was not detectable after 72 h. Collectively, the hypoglycemic effects of CEMC suggest that it has potential for increasing insulin sensitivity in patients with T2D rather than for protecting patients with T1D against β-cell dysfunction.

KEYWORDS:

Charantin; Hypoglycemic; Insulin signaling; Momordica charantia; Pancreatic β cells; Type 2 diabetes

PMID:
24751968
DOI:
10.1016/j.fct.2014.04.008
[Indexed for MEDLINE]

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