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咖啡因可减轻饮食诱导肥胖大鼠的代谢综合征。

Caffeine attenuates metabolic syndrome in diet-induced obese rats.

机构信息

Department of Biological and Physical Sciences, University of Southern Queensland, Toowoomba, Queensland, Australia.

出版信息

Nutrition. 2012 Oct;28(10):1055-62. doi: 10.1016/j.nut.2012.02.013. Epub 2012 Jun 19.

DOI:10.1016/j.nut.2012.02.013
PMID:22721876
Abstract

OBJECTIVE

Caffeine is a constituent of many non-alcoholic beverages. Pharmacological actions of caffeine include the antagonism of adenosine receptors and the inhibition of phosphodiesterase activity. The A₁ adenosine receptors present on adipocytes are involved in the control of fatty acid uptake and lipolysis. In this study, the effects of caffeine were characterized in a diet-induced metabolic syndrome in rats.

METHODS

Rats were given a high-carbohydrate, high-fat diet (mainly containing fructose and beef tallow) for 16 wk. The control rats were given a corn starch diet. Treatment groups were given caffeine 0.5 g/kg of food for the last 8 wk of the 16-wk protocol. The structure and function of the heart and the liver were investigated in addition to the metabolic parameters including the plasma lipid components.

RESULTS

The high-carbohydrate, high-fat diet induced symptoms of metabolic syndrome, including obesity, dyslipidemia, impaired glucose tolerance, decreased insulin sensitivity, and increased systolic blood pressure, associated with the development of cardiovascular remodeling and non-alcoholic steatohepatitis. The treatment with caffeine in the rats fed the high-carbohydrate, high-fat diet decreased body fat and systolic blood pressure, improved glucose tolerance and insulin sensitivity, and attenuated cardiovascular and hepatic abnormalities, although the plasma lipid concentrations were further increased.

CONCLUSION

Decreased total body fat, concurrent with increased plasma lipid concentrations, reflects the lipolytic effects of caffeine in adipocytes, likely owing to the caffeine antagonism of A₁ adenosine receptors on adipocytes.

摘要

目的

咖啡因是许多非酒精饮料的组成成分。咖啡因的药理作用包括拮抗腺嘌呤受体和抑制磷酸二酯酶活性。脂肪细胞上的 A₁ 腺嘌呤受体参与脂肪酸摄取和脂肪分解的控制。在这项研究中,研究了咖啡因在大鼠饮食诱导的代谢综合征中的作用。

方法

大鼠给予高碳水化合物、高脂肪饮食(主要含有果糖和牛脂)16 周。对照组大鼠给予玉米淀粉饮食。治疗组在 16 周方案的最后 8 周给予 0.5 g/kg 食物的咖啡因。除了代谢参数(包括血浆脂质成分)外,还研究了心脏和肝脏的结构和功能。

结果

高碳水化合物、高脂肪饮食可诱导代谢综合征症状,包括肥胖、血脂异常、葡萄糖耐量受损、胰岛素敏感性降低和收缩压升高,同时伴有心血管重构和非酒精性脂肪性肝炎的发展。在给予高碳水化合物、高脂肪饮食的大鼠中,咖啡因治疗可降低体脂肪和收缩压,改善葡萄糖耐量和胰岛素敏感性,并减轻心血管和肝脏异常,尽管血浆脂质浓度进一步升高。

结论

全身脂肪减少,同时血浆脂质浓度升高,反映了咖啡因在脂肪细胞中的脂肪分解作用,可能归因于咖啡因对脂肪细胞上的 A₁ 腺嘌呤受体的拮抗作用。

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