Martin Joseph V, Nolan Bonnie, Wagner George C, Fisher Hans
Biology Department, 315 Penn Street, Rutgers University, Camden, NJ 08102, USA.
Med Sci Monit. 2004 Dec;10(12):BR455-61.
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.
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.
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.
在大鼠存在或不存在酒精摄入的情况下,研究了咖啡因对高脂(低碳水化合物)饮食诱导的脂肪肝的影响。
材料/方法:雄性 Long-Evans 大鼠在两到十二周的时间内,给予能量含量平衡但脂肪和碳水化合物含量不同的无酒精或含酒精液体饮食。此外,几个组的液体饮食中含有 0.05% 的咖啡因。实验结束时,采集躯干血用于检测血糖和血浆瘦素,称量附睾脂肪垫重量,并取肝脏分析糖原、葡萄糖和脂肪。
与相应的无乙醇饮食相比,含乙醇饮食增加了肝脏脂肪,消耗了肝脏糖原和葡萄糖,但与高脂饮食的大鼠相比,高碳水化合物饮食的大鼠这些影响较轻。饮食中添加 0.05% 的咖啡因增加了有跑步机的动物的运动活性,但对乙醇诱导的肝脏葡萄糖消耗和脂肪肝诱导没有保护作用。事实上,咖啡因似乎会加剧乙醇消耗肝脏糖原、降低附睾脂肪垫重量和降低血清瘦素的作用。
由于咖啡因等处理可消耗肝脏糖原储备,但不会加剧乙醇相关的肝脏脂肪积累,因此慢性乙醇摄入后肝脏糖原的消耗不是导致脂肪肝的唯一因果决定因素。碳水化合物代谢的其他方面,包括内源性调节中间体或乙醇衍生化合物的积累,可能更直接地受到慢性酒精摄入的影响。