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通过 AMP 激活蛋白激酶信号通路,咖啡因和儿茶素对慢性喂养小鼠脂代谢的协同作用。

Synergistic effects of caffeine and catechins on lipid metabolism in chronically fed mice via the AMP-activated protein kinase signaling pathway.

机构信息

Jiangxi Key Laboratory of Natural Product and Functional Food, College of Food Science and Engineering, Jiangxi Agricultural University, Nanchang, 330045, China.

Library of Jiangxi Agricultural University, Nanchang, 330045, China.

出版信息

Eur J Nutr. 2017 Oct;56(7):2309-2318. doi: 10.1007/s00394-016-1271-4. Epub 2016 Jul 21.

Abstract

PURPOSE

To investigate the mechanistic effects of combined exposure to caffeine and catechins on lipid metabolism in mice.

METHODS

Seventy mice were randomly assigned to seven groups and fed diets containing varying doses of caffeine and catechins for 24 weeks. Body weight gain, intraperitoneal adipose tissue (IPAT) weight, serum biochemical parameters, and enzymatic activities, mRNA and protein expression levels of lipid metabolism-related enzymes in the liver and IPAT were analyzed.

RESULTS

Following administration of caffeine and catechins, body weight gain, IPAT weight, serum and liver concentrations of total cholesterol and triglyceride were markedly reduced. Lipase activities, including that of AMP-activated protein kinase (AMPK), acyl-CoA oxidase, carnitine acyltransferase, adipose triglyceride lipase, and hormone-sensitive lipase, were significantly upregulated; however, fatty acid synthase (FAS) activity in the liver was suppressed. Combined exposure to caffeine and catechins significantly upregulated mRNA and protein expression levels of lipases while downregulating FAS mRNA expression and protein expression of peroxisome proliferator-activated receptor γ2.

CONCLUSIONS

The combination of caffeine and catechins regulated the enzymatic activities, mRNA, and protein expression levels of lipid metabolism-related enzymes, resulting in suppression of body weight gain and IPAT weight in mice, potentially through activation of the AMPK signaling pathway. This study indicates that chronic intake of both caffeine and catechins can synergistically contribute to prevention of obesity and lifestyle-related diseases.

摘要

目的

研究咖啡因和儿茶素联合暴露对小鼠脂代谢的作用机制。

方法

将 70 只小鼠随机分为 7 组,给予不同剂量的咖啡因和儿茶素喂养 24 周。分析体重增加、腹腔脂肪组织(IPAT)重量、血清生化参数、肝和 IPAT 中与脂代谢相关的酶的酶活性、mRNA 和蛋白表达水平。

结果

给予咖啡因和儿茶素后,体重增加、IPAT 重量、血清和肝脏总胆固醇和甘油三酯浓度明显降低。脂肪酶活性,包括 AMP 激活蛋白激酶(AMPK)、酰基辅酶 A 氧化酶、肉碱酰基转移酶、脂肪甘油三酯脂肪酶和激素敏感脂肪酶,均显著上调;然而,肝脏中的脂肪酸合成酶(FAS)活性受到抑制。咖啡因和儿茶素联合暴露显著上调了脂肪酶的 mRNA 和蛋白表达水平,同时下调了过氧化物酶体增殖物激活受体 γ2 的 FAS mRNA 表达和蛋白表达。

结论

咖啡因和儿茶素的联合作用调节了与脂代谢相关的酶的酶活性、mRNA 和蛋白表达水平,导致小鼠体重增加和 IPAT 重量减轻,可能通过激活 AMPK 信号通路。本研究表明,长期摄入咖啡因和儿茶素可能协同预防肥胖和与生活方式相关的疾病。

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