Gold thioglucose damage to the satiety center: inhibition in diabetes

Abstract

A comparison was made between control and diabetic mice with respect to the effi ;t of gold thioglucose on the hypothalamics satiety center. Contr 1 mice given gold thioglucose showed gold deposition and lesions h the satiety center and exhibited hyperphagia and obesity. Alloxan diabetes inhibited deposition of gold and formation of lesions. Extreme hyperphagia was present in alloxan-diabetic mice not given gold thioglucose; the administration of gold thioglucose to such mice did not alter the existing hyperphagia nor did it bring about obesity. Like mice made diabetic by alloxan, mice made diabetic by the administration of guinea pig anti-insulin serum were resistant to gold thioglucose-induced lesions of the satiety center. Anti-insulin-diabetic mice given gold thioglucose and then allowed to recover from the diabetes, did not become obese. It is postulated that insulin deficiency, directly or through effects on circulating metabolites, decreases the uptake of gold thioglucose by the satiety center.