Epigallocatechin-3-Gallate-Rich Green Tea Extract Ameliorates Fatty Liver and Weight Gain in Mice Fed a High Fat Diet by Activating the Sirtuin 1 and AMP Activating Protein Kinase Pathway

Author:

Bae Ui-Jin12,Park John3,Park Il Woon4,Chae Byung Min5,Oh Mi-Ra2,Jung Su-Jin2,Ryu Geon-Seek6,Chae Soo-Wan72,Park Byung-Hyun1

Affiliation:

1. Department of Biochemistry, Chonbuk National University Medical School, Jeonju, Jeonbuk 54896, South Korea

2. Clinical Trial Center for Functional Foods, Chonbuk National University Hospital, Jeonju, Jeonbuk 54907, South Korea

3. Department of Chemistry, Chonbuk National University, Jeonju, Jeonbuk 54896, South Korea

4. Department of Cognitive Science, Case Western Reserve University, Cleveland, OH 44106, USA

5. Division of Biotechnology, College of Environmental and Bioresource Sciences, Chonbuk National University, Iksan, Jeonbuk 54596, South Korea

6. AlnO Food Inc., Daejeon 34015, South Korea

7. Department of Pharmacology, Chonbuk National University Medical School, Jeonju, Jeonbuk 54896, South Korea

Abstract

The prevalence of metabolic diseases has risen globally in parallel with the obesity epidemic over the past few decades. Green tea has been reported to have metabolically beneficial effects on obesity; however, the mechanism by which green tea regulates lipid metabolism is not clearly understood. Male c57BL/6 mice were fed a normal chow diet, a high-fat diet (HFD), or an HFD supplemented with various doses of epigallocatechin gallate-rich green tea extract (GTE) for 12 weeks. GTE supplementation reduced body weight gain, prevented hepatic fat accumulation, decreased hypertriglyceridemia, and improved hyperglycemia and insulin resistance in HFD-fed mice. The underlying mechanisms of these beneficial effects of GTE might involve the upregulation of sirtuin 1 and AMP activated protein kinase (AMPK) and the downregulation of enzymes related to de novo lipogenesis. Consistent with the in vivo findings, GTE increased the expression and activity of sirtuin 1, enhanced the binding of sirtuin 1 to liver kinase B1 (LKB1) and subsequent deacetylation of LKB1, and reduced triglyceride accumulation in HepG2 cells. These results suggest the possible therapeutic potential of dietary epigallocatechin gallate-rich GTE supplementation for preventing the development and progression of hepatic steatosis and obesity.

Publisher

World Scientific Pub Co Pte Lt

Subject

Complementary and alternative medicine,General Medicine

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