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Biomed Pharmacother. 2017 Mar;87:73-81. doi: 10.1016/j.biopha.2016.12.082. Epub 2016 Dec 29.

Green tea epigallocatechin 3-gallate alleviates hyperglycemia and reduces advanced glycation end products via nrf2 pathway in mice with high fat diet-induced obesity.

Author information

1
Department of Human Nutrition, College of HealthSciences, Qatar University, Doha, 2713, Qatar.
2
Laboratory for Functional Foods and Human Health, Center for Excellence in Post-Harvest Technologies, North Carolina Agricultural and Technical State University, North Carolina Research Campus, 500 Laureate Way, Kannapolis, NC 28081, United States.
3
Department of Human Nutrition, College of HealthSciences, Qatar University, Doha, 2713, Qatar. Electronic address: ahmedna@qu.edu.qa.

Abstract

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.

KEYWORDS:

Advance glycation end-products; Diabetes; Dicarbonyl stress; Epigallocatechin gallate; Nrf2; RAGE

PMID:
28040599
DOI:
10.1016/j.biopha.2016.12.082
[Indexed for MEDLINE]

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