Hyperphagia in rats with experimental diabetes mellitus: a response to a decreased supply of utilizable fuels.
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.
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001823:Body Composition; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000178:diet therapy; D004032:Diet; D004040:Dietary Carbohydrates; D004041:Dietary Fats; D004734:Energy Metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005247:Feeding Behavior / Q000502:physiology*; D005260:Female; D006029:Glycosuria; D007328:Insulin / Q000097:blood; D007657:Ketone Bodies / Q000652:urine; D008112:Liver Glycogen / Q000032:analysis; D008297:Male; D051381:Rats
D001786:Blood Glucose; D004040:Dietary Carbohydrates; D004041:Dietary Fats; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D007657:Ketone Bodies; D008112:Liver Glycogen