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AuthorSampath, Chethan
AuthorRashid, Muhammed Raihan
AuthorSang, Shengmin
AuthorAhmedna, Mohamed
Available date2017-02-22T11:31:08Z
Publication Date2017-03-01
Publication NameBiomedicine & Pharmacotherapy
Identifierhttp://dx.doi.org/10.1016/j.biopha.2016.12.082
CitationChethan Sampatha, Muhammed Raihan Rashida, Shengmin Sangb, Mohamed Ahmednaa. “Green tea epigallocatechin 3-gallate alleviates hyperglycemia and reduces advanced glycation end products via nrf2 pathway in mice with high fat diet-induced obesity”, Volume 87, pp. 73-81
ISSN07533322
URIhttp://www.sciencedirect.com/science/article/pii/S0753332216319928
URIhttp://hdl.handle.net/10576/5300
AbstractAbstract Epigallocatechin 3-gallate (EGCG) from green tea may reduce plasma glucose and alleviate complications of diabetes by attenuating advanced glycation end products (AGEs) formation. We hypothesized that EGCG would mitigate AGEs formation via activating the nuclear factor erythroid-2-related-factor-2 (Nrf2) pathway in a mouse model of high fat diet-induced obesity. Dietary EGCG was tested in C57BL/6 mice that were placed on a high-fat diet with or without ECGC for 17 weeks and compared to a control group placed on low-fat diet for the same period. Weight gain and fasting blood glucose were measured throughout the study duration. Supplementation of high fat diet with dietary EGCG significantly reduced weight gain, plasma glucose, insulin level, liver and kidney weight. EGCG administration also decreased the levels of AGEs in both plasma and liver while inhibiting the receptor for AGE (RAGE) expression of, activating Nrf2 and enhancing GSH/GSSG ratio compared to mice on high fat diet without added EGCG. This study demonstrated that EGCG has the potential to help control hyperglycemia, reduce weight, and alleviate diabetes complications.
SponsorQatar National Research Fund
Languageen
PublisherElsevier
SubjectDiabetes
Advance glycation end-products
Epigallocatechin gallate
Nrf2
Dicarbonyl stress
RAGE
TitleGreen tea epigallocatechin 3-gallate alleviates hyperglycemia and reduces advanced glycation end products via nrf2 pathway in mice with high fat diet-induced obesity
TypeArticle
Pagination73-81
Volume Number87


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