Friedman M I
J Comp Physiol Psychol. 1978 Feb;92(1):109-17. doi: 10.1037/h0077431.
Alloxan-diabetic rats were hyperphagic when fed diets containing little fat, but they ate normal amounts of food when given diets rich in fat. Normal rats increased food intake to the same degree when the caloric density of their diet was decreased by reducing the content of fats or carbohydrates in isocaloric amounts. Diabetic rats did not respond substantially to changes in caloric density of their diet which were produced by altering the content of dietary carbohydrates, but they systematically increased food intake as the amount of fat in their diet was reduced. Diabetic rats ate normal amounts of a high-fat diet despite continued loss of nutrients in urine and persisting impairments in glucose utilization, fat storage, and liver glycogen deposition. These findings suggest that hyperphagia in experimental diabetes mellitus is a compensatory response to a lack of utiliziable fat fuels rather than the result of a metabolic disturbance per se.
四氧嘧啶糖尿病大鼠在喂食低脂饮食时会出现食欲亢进，但当给予富含脂肪的饮食时，它们的食量正常。当正常大鼠的饮食热量密度通过等量减少脂肪或碳水化合物含量而降低时，它们的食物摄入量会增加到相同程度。糖尿病大鼠对通过改变饮食碳水化合物含量所产生的饮食热量密度变化没有明显反应，但随着饮食中脂肪量的减少，它们会系统性地增加食物摄入量。尽管糖尿病大鼠持续通过尿液流失营养物质，且在葡萄糖利用、脂肪储存和肝糖原沉积方面仍存在持续损伤，但它们对高脂饮食的食量正常。这些发现表明，实验性糖尿病中的食欲亢进是对缺乏可利用脂肪燃料的一种代偿反应，而非代谢紊乱本身的结果。
