Del Prete E, Lutz T A, Scharrer E
Institute of Veterinary Physiology, University of Z ürich, Zürich, Switzerland.
Appetite. 2000 Apr;34(2):137-45. doi: 10.1006/appe.1999.0303.
The present study investigates the mechanisms underlying the transient hypophagia occurring when rats adapted to high-fat, carbohydrate-free diets are switched to high-carbohydrate, low-fat diets. The hypophagia after the high-fat, carbohydrate-free to high-carbohydrate, low-fat diet shift seems to depend on the amount of carbohydrate in the diet, since an attenuation of hypophagia was observed when high-fat, carbohydrate-free-adapted rats were switched to a medium-carbohydrate, medium-fat diet. A role of glucose intolerance in the hypophagia is supported by the attenuation of carbohydrate anorexia in rats adapted to a high-fat diet containing n -3 polyunsaturated fatty acids from fish oil (60% of fat as fish oil), which has been shown to improve glucose tolerance in rats. Furthermore, the increased plasma glucose concentration in the high-fat, carbohydrate-free diet to high-carbohydrate, low-fat shifted rats despite the suppression in food intake also suggests an involvement of glucose intolerance in the hypophagia. The failure of the inhibitor of hepatic-fatty-acid oxidation mercaptoacetate (400 micromol/kg, i.p.) to counteract carbohydrate anorexia in the HF-adapted rats argues against an involvement of fatty-acids oxidation in the inhibition of eating after high-fat, carbohydrate-free to high-carbohydrate, low-fat diet shift. This is also supported by the failure to demonstrate a relationship between plasma beta-hydroxybutyrate and the severity of the hypophagia. A role of leptin in the hypophagia seems unlikely, since plasma leptin after diet shift was unchanged. Ingestion of the high-carbohydrate, low-fat diet also produced an aversion towards this diet in high-fat, carbohydrate-free-adapted rats. It is concluded that the transient hypophagia induced by switching rats from a high-fat to a high-carbohydrate diet is not related to fatty acid oxidation but to transiently impaired carbohydrate utilization.
本研究探讨了适应高脂、无碳水化合物饮食的大鼠转而食用高碳水化合物、低脂饮食时发生短暂性摄食减少的潜在机制。从高脂、无碳水化合物饮食转变为高碳水化合物、低脂饮食后的摄食减少似乎取决于饮食中的碳水化合物含量，因为当适应高脂、无碳水化合物饮食的大鼠转而食用中等碳水化合物、中等脂肪饮食时，摄食减少现象有所减轻。适应含来自鱼油的n -3多不饱和脂肪酸（脂肪的60%为鱼油）的高脂饮食的大鼠，其碳水化合物厌食症有所减轻，这支持了葡萄糖不耐受在摄食减少中起作用，且已证明该饮食可改善大鼠的葡萄糖耐受性。此外，尽管食物摄入量受到抑制，但从高脂、无碳水化合物饮食转变为高碳水化合物、低脂饮食的大鼠血浆葡萄糖浓度升高，这也表明葡萄糖不耐受与摄食减少有关。肝脂肪酸氧化抑制剂巯基乙酸盐（400微摩尔/千克，腹腔注射）未能抵消适应高脂饮食大鼠的碳水化合物厌食症，这表明脂肪酸氧化与从高脂、无碳水化合物饮食转变为高碳水化合物、低脂饮食后进食抑制无关。血浆β-羟基丁酸与摄食减少严重程度之间未显示出相关性也支持了这一点。瘦素在摄食减少中似乎不太可能起作用，因为饮食转变后血浆瘦素未发生变化。在适应高脂、无碳水化合物饮食的大鼠中，摄入高碳水化合物、低脂饮食也会使其对这种饮食产生厌恶。得出的结论是，将大鼠从高脂饮食转变为高碳水化合物饮食所诱导的短暂性摄食减少与脂肪酸氧化无关，而是与碳水化合物利用的短暂受损有关。
