Beneficial effects of tea catechins on diet-induced obesity: stimulation of lipid catabolism in the liver

被引：400

作者：

Murase, T ^{[1
]}

Nagasawa, A ^{[1
]}

Suzuki, J ^{[1
]}

Hase, T ^{[1
]}

Tokimitsu, I ^{[1
]}

机构：

[1] Kao Corp, Biol Sci Labs, Tochigi 3213497, Japan

来源：

INTERNATIONAL JOURNAL OF OBESITY | 2002年 / 26卷 / 11期

关键词：

tea catechins; obesity; visceral fat; liver fat; beta-oxidation;

D O I：

10.1038/sj.ijo.0802141

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

OBJECTIVE: Obesity has increased at an alarming rate in recent years and is now a worldwide health problem. We investigated the effects of long-term feeding with tea catechins, which are naturally occurring polyphenolic compounds widely consumed in Asian countries, on the development of obesity in C57BL/6J mice. DESIGN: We measured body weight, adipose tissue mass and liver fat content in mice fed diets containing either low-fat (5% triglyceride (TG)), high-fat (30% TG), or high-fat supplemented with 0.1 - 0.5% (w/w) tea catechins for 11 months. The beta-oxidation activities and related mRNA levels were measured after 1 month of feeding. RESULTS: Supplementation with tea catechins resulted in a significant reduction of high-fat diet-induced body weight gain, visceral and liver fat accumulation, and the development of hyperinsulinemia and hyperleptinemia. Feeding with tea catechins for 1 month significantly increased acyl-CoA oxidase and medium chain acyl-CoA dehydrogenase mRNA expression as well as beta-oxidation activity in the liver. CONCLUSION: The stimulation of hepatic lipid metabolism might be a factor responsible for the anti-obesity effects of tea catechins. The present results suggest that long-term consumption of tea catechins is beneficial for the suppression of diet-induced obesity, and it may reduce the risk of associated diseases including diabetes and coronary heart disease.

引用

页码：1459 / 1464

页数：6

共 26 条

[1] Peroxisome proliferator-activated receptor α negatively regulates the vascular inflammatory gene response by negative cross-talk with transcription factors NF-κB and AP-1 [J].