Black tea affects obesity by reducing nutrient intake and activating AMP-activated protein kinase in mice
文献类型: 外文期刊
作者: Pan, Shunshun 1 ; Deng, Xuming 1 ; Sun, Shili 2 ; Lai, Xingfei 2 ; Sun, Lingli 2 ; Li, Qiuhua 3 ; Xiang, Limin; Zhang, 1 ;
作者机构: 1.South China Agr Univ, Coll Hort, Dept Tea Sci, 483 Wushan Rd, Guangzhou 510642, Guangdong, Peoples R China
2.Guangdong Acad Agr Sci, Res Inst, Guangdong Prov Key Lab Tea Plant Resources Innova, Guangzhou 510640, Guangdong, Peoples R China
3.Guangdong Acad Agr Sci, Res Inst, Guangdong Prov Key Lab Tea Plant R
关键词: Yinghong NO. 9 black tea; Anti-obesity; AMP-activated protein kinase; Inflammation
期刊名称:MOLECULAR BIOLOGY REPORTS ( 影响因子:2.316; 五年影响因子:2.357 )
ISSN: 0301-4851
年卷期: 2018 年 45 卷 5 期
页码:
收录情况: SCI
摘要: The effects of certain tea components on the prevention of obesity in humans have been reported recently. However, whether Yinghong NO. 9 black tea consumption has beneficial effects on obesity are not known. Here, we obtained a Yinghong NO. 9 black tea infusion (Y9 BTI) and examined the anti-obesity effects of its oral administration. ICR mice were fed a standard diet supplemented with Y9 BTI at 0.5, 1.0, or 2.0 g/kg body weight for two weeks, and the body weight were recorded. HE staining was used to evaluate the effect of Y9 BTI on mice liver. Western blot analysis was used to detect the expression levels of related proteins in the mice liver and adipose. We found that the body weights of the mice in the control group were significantly higher than those of the mice in the middle and high dose groups. The results of western blot showed that Y9 BTI up-regulated the expression of liver kinase B1 (LKB1) and adenosine monophosphate-activated protein kinase (AMPK) and also increased in AMPK phosphorylation (p-AMPK) and LKB1 phosphorylation (p-LKB1). Y9 BTI significantly down-regulated Fas Cell Surface Death Receptor(FAS) and activated the phosphorylation of acetyl-CoA carboxylase (ACC). Furthermore, Y9 BTI (2.0 g/kg BW) down-regulated the expression of three factors (IL-1 beta, Cox-2, and iNOS). Altogether, Y9 BTI supplementation reduced the feed intake of mice and may prevent obesity by inhibiting lipid absorption. These results suggest that Y9 BTI may regulate adipogenic processes through the LKB1/AMPK pathway.
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