Specific loss of the hypoglycemic control of feeding in recovered lateral rats

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Abstract
Rats that are eating and regulating food intake after recovery from the initial aphagia and anorexia of lateral hypothalamic lesions do not eat more during insulin-induced hypoglycemia. The deficit is specific. They do increase food intake in response to dilution of the diet and to low ambient temperature. And the deficit is permanent. It is present in animals surviving for as long as 503 days after surgery. An essential portion of the neurologic system that mobilizes feeding in response to decreases in blood sugar is therefore focused in the lateral hypothalamus and immediately adjacent structures. Rats with ventromedial hypothalamic damage sufficient to produce hyperphagia and obesity do eat more in response to hypoglycemia. The medial hypothalamic glucoreceptive system that may participate in the control of feeding is therefore not an essential part of the mechanism proposed here. In discussion, the specific impairment of the hypoglycemic control of feeding is contrasted with the global impairment of the regulatory controls of drinking that is produced by the same lesions.