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. 2008 Sep;138(9):1677-83.
doi: 10.1093/jn/138.9.1677.

The major green tea polyphenol, (-)-epigallocatechin-3-gallate, inhibits obesity, metabolic syndrome, and fatty liver disease in high-fat-fed mice

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The major green tea polyphenol, (-)-epigallocatechin-3-gallate, inhibits obesity, metabolic syndrome, and fatty liver disease in high-fat-fed mice

Mousumi Bose et al. J Nutr. 2008 Sep.

Abstract

In this study, we investigated the effects of the major green tea polyphenol, (-)-epigallocatechin-3-gallate (EGCG), on high-fat-induced obesity, symptoms of the metabolic syndrome, and fatty liver in mice. In mice fed a high-fat diet (60% energy as fat), supplementation with dietary EGCG treatment (3.2 g/kg diet) for 16 wk reduced body weight (BW) gain, percent body fat, and visceral fat weight (P < 0.05) compared with mice without EGCG treatment. The BW decrease was associated with increased fecal lipids in the high-fat-fed groups (r(2) = 0.521; P < 0.05). EGCG treatment attenuated insulin resistance, plasma cholesterol, and monocyte chemoattractant protein concentrations in high-fat-fed mice (P < 0.05). EGCG treatment also decreased liver weight, liver triglycerides, and plasma alanine aminotransferase concentrations in high-fat-fed mice (P < 0.05). Histological analyses of liver samples revealed decreased lipid accumulation in hepatocytes in mice treated with EGCG compared with high-fat diet-fed mice without EGCG treatment. In another experiment, 3-mo-old high-fat-induced obese mice receiving short-term EGCG treatment (3.2 g/kg diet, 4 wk) had decreased mesenteric fat weight and blood glucose compared with high-fat-fed control mice (P < 0.05). Our results indicate that long-term EGCG treatment attenuated the development of obesity, symptoms associated with the metabolic syndrome, and fatty liver. Short-term EGCG treatment appeared to reverse preexisting high-fat-induced metabolic pathologies in obese mice. These effects may be mediated by decreased lipid absorption, decreased inflammation, and other mechanisms.

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Figures

FIGURE 1
FIGURE 1
Effect of long-term EGCG treatment (16 wk) on BW (A,C), visceral fat weight (B,D), and blood glucose (E) in high-fat–fed C57BL/6 mice. Blood glucose was measured in food-deprived mice. Data are means ± SEM. Labeled means at a time without a common letter differ, P < 0.05.
FIGURE 2
FIGURE 2
Effect of long-term EGCG treatment (16 wk) on fatty liver in high-fat–fed C57BL/6J mice. Gross examination of liver samples from LF, HF, and HFE mice (A). Histological examination of liver samples from LF (B), HF (C), and HFE (D) mice, shown at 5× magnification.
FIGURE 3
FIGURE 3
Effect of short-term EGCG treatment (4 wk) on BW (A,B), visceral fat weight (C), and blood glucose (D) in high-fat–fed C57BL/6J mice. Blood glucose was measured in food-deprived mice. Data are means ± SEM. Labeled means at a time without a common letter differ, P < 0.05 (Expt. 3).

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