The hypothalamic control of food intake in rats
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The effect on feeding behaviour in the rat, of perm anent electrolytic lesions in the hypothalam us which cause obesity, has been studied. Soon after operation, the animals were extremely voracious. As the obesity became established, the voracity was reduced in degree and finally disappeared. Young unoperated rats could not be made to exhibit such voracity even after starvation. The young unoperated animals showed little discrimination against unattractive diets. When fed on meal mixed with an equal weight of kaolin, they obtained a normal nutrient intake, and maintained their weight by doubling the bulk eaten. In the voracious stage, operated animals adapted in this way more quickly than normal; in the obese stage they adapted more slowly and only after loss of considerable body fat. Older unoperated animals, which were moderately obese, resembled the operated ones in their feeding reactions. It is suggested that the effect of hypothalamic damage is to emphasize two components of the urge to eat, a primitive voracious one, and a more discriminative component, either of which may be dominant according to the state of the fat stores. The simplicity of the young rats’ reactions appears to be due to closer co-ordination of these components by the hypothalam us. Modification of the hypothalamic control of energy intake may be a pre-requisite of obesity in general. Reasons are advanced for regarding the hypothalamic mechanism as being sensitive to chemical changes in the blood.