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Effects of dietary caffeine and alcohol on liver carbohydrate and fat metabolism in rats

机译:饮食中咖啡因和酒精对大鼠肝脏碳水化合物和脂肪代谢的影响

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Background:The effects of caffeine on fatty liver induced by high-fat (low-carbohydrate) diets were examined in the presence or absence of alcohol consumption by rats.Material/Methods:For periods ranging from two to twelve weeks, male Long-Evans rats were given alcohol-free or alcohol-containing liquid diets balanced for energy content, but varying in fat and carbohydrate. In addition, several of the groups were given 0.05% caffeine as a constituent of the liquid diet. At the end of the experiments, trunk blood was collected for blood glucose and plasma leptin, epididymal fat pads were weighed, and liver was taken for analysis of glycogen, glucose, and fat.Results:Ethanol-containing diets increased liver fat and depleted liver glycogen and glucose as compared to the corresponding ethanol-free diets, but these effects were less severe in rats given high-carbohydrate diets as compared to those maintained on the high-fat diet. The inclusion of 0.05% caffeine in the diet increased the motor activity of animals with access to a running wheel, yet had no protective effect against ethanol-induced depletion of liver glucose and induction of fatty liver. In fact, caffeine appears to exacerbate the effect of ethanol to deplete liver glycogen, decrease epididymal fat pad weight and lower serum leptin.Conclusions:Since liver glycogen stores can be depleted by treatments such as caffeine which do not exacerbate ethanol-related liver fat accumulation, the depletion of liver glycogen following chronic ethanol is not the single causal determinant of the resulting fatty liver. Other aspects of carbohydrate metabolism, including accumulations of endogenous regulatory intermediates or ethanol-derived compounds, might be more directly influenced by chronic alcohol ingestion.
机译:背景:研究了咖啡因对高脂肪(低碳水化合物)饮食诱导的脂肪肝的影响,方法是在有或没有饮酒的情况下进行大鼠研究。材料/方法:在两到十二周的时间里,雄性长埃文斯犬给予大鼠无酒精或含酒精的流质饮食,使其能量含量保持平衡,但脂肪和碳水化合物的含量却有所不同。另外,一些组被给予0.05%咖啡因作为流质饮食的成分。实验结束时,采集躯干血液以测定血糖和血浆瘦素,称重附睾脂肪垫,并取肝进行糖原,葡萄糖和脂肪的分析。结果:含乙醇的饮食会增加肝脏脂肪和肝脏消耗糖原和葡萄糖与相应的无乙醇饮食相比,但与高脂饮食相比,这些影响在给予高碳水化合物饮食的大鼠中不那么严重。饮食中加入0.05%咖啡因可增加动物的运动能力,但不能抵抗乙醇诱导的肝葡萄糖消耗和脂肪肝的诱导。事实上,咖啡因似乎加剧了乙醇消耗肝糖原,降低附睾脂肪垫重量和降低血清瘦素的作用。结论:由于咖啡因等治疗可消耗肝糖原,因此不会加剧乙醇相关的肝脂肪积聚。 ,慢性乙醇后肝糖原的耗竭不是导致脂肪肝的唯一原因。碳水化合物的代谢的其他方面,包括内源性调节中间体或乙醇衍生化合物的积累,可能会受到长期饮酒的直接影响。

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