Transient hypophagia in rats switched from high-fat diets with different fatty-acid pattern to a high-carbohydrate diet.
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.
Del Prete
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Institute of Veterinary Physiology, University of Z ürich, Zürich, Switzerland.
Lutz
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TA
Scharrer
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D000704:Analysis of Variance; D000818:Animals; D001786:Blood Glucose / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D004032:Diet; D004040:Dietary Carbohydrates / Q000008:administration & dosage* / Q000494:pharmacology; D004041:Dietary Fats / Q000008:administration & dosage* / Q000494:pharmacology; D005231:Fatty Acids, Unsaturated / Q000008:administration & dosage; D001068:Feeding and Eating Disorders / Q000209:etiology*; D020738:Leptin / Q000097:blood; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013649:Taste
D001786:Blood Glucose; D004040:Dietary Carbohydrates; D004041:Dietary Fats; D005231:Fatty Acids, Unsaturated; D020738:Leptin