Abstract
Weanling rats received bilateral electrolytic lesions in the ventromedial (VMN) or dorsomedial (DMN) hypothalamic nuclei; sham‐operated rats served as controls. The animals were maintained under standard conditions for 13–;17 days post‐operatively and killed by decapitation. In addition, to measurements of weight gain and linear growth, Lee Index, and food intake, and activities of several hepatic enzymes and hepatic protein content were determined in untreated rats and in animals injected with 20 mg/kg cortisol 4 hours prior to sacrifice. In accordance with previously established data, weanling rats with VMN lesions did not gain more weight or eat more than their controls but became obese and retarded in linear growth. Weanling rats with DMN lesions showed both reduced ponderal and linear growth and were hypophagic but had normal body composition. Rats with VMN lesions had significantly increased activities of alanine transaminase (AT), serine dehydratase (SD), and hepatic protein; tryptophan oxygenase (TO) was decreased. In VMN‐lesioned rats treatment with cortisol decreased tyrosine aminotransferase (TKT) and liver protein. Lesions in the DMN increased AT and liver protein but left TKT unchanged. Cortisol induced TO and TKT in comparison with vehicle‐treated DMN rats. In another experiment, hepatic alanine tranaminase (AT) and fructose‐1,6,diphophatase (FDPase) were found to be elevated, but levels of pyruvate carboxylase (PC), phosphoenolpyruvate carboxykinase (PEPCK), and plasma glucagon were normal in rats with VMN lesions. The failure to find changes in 2 key gluconeogenic enzymes suggests that the enhanced gluconeogenesis in VMN rats demonstrated in a previous study depends more on substrate availability than on changes in enzyme activity. The data suggest that the central nervous system plays a role in the regulation of certain enzymes involved in protein metabolism.