The rate of gluconeogenesis was similar in liver of both fed heat acclimated and control hamsters. 24 hr of fasting caused 6 times elevation in hepatic gluconeogenesis of the control animals whereas only 4 times enhancement of this pathway was found in heat acclimated animals. Thus, significant difference existed between the two experimental groups in fasting. Triiodothyronine stimulated the rate of gluconeogenesis only in fed heat acclimated hamsters whereas dibutyryl cyclic AMP caused elevation of this pathway in liver slices of fed control hamsters only. The results suggest that a decrease in hepatic gluconeogenesis in heat acclimation occurs only in fasted animals and it is controlled by thyroid hormones.