Adaptive thermogenesis is the dissipation of energy through heat production and occurs in specialised tissues including brown adipose tissue and skeletal muscle. Our work aims to characterise endocrine factors that regulate thermogenesis in these two tissues. In order to address this, we developed an ovine model. We demonstrate that post-prandial thermogenesis is evoked in sheep by meal feeding, where food is restricted to a set daily meal time. With this, we have characterised sex differences and the effects of sex and stress steroids on thermogenesis in muscle and fat. We show that testosterone reduces thermogenesis in both tissues in males but not females. On the other hand, estrogen increases heat production in both tissues in females. Thus the control of thermogenesis is sexually dimorphic and affected by sex steroids.
In addition, we determined whether differences in thermogenesis alter predisposition to obesity. To address this we developed a model that used cortisol responsiveness as a marker for predisposition to obesity. Using a synacthen (ACTH) challenge, animals were characterised as either high or low cortisol responders (HR and LR). Animals characterised as HR have greater propensity to become obese when placed on a high energy diet, but this is not due to a difference in food intake. LR animals have a greater thermogenic capacity than HR animals and this confers relative protection against obesity. Interestingly, the differences in thermogenesis are localised to skeletal muscle and do not occur in adipose tissue.
In conclusion, the regulation of thermogenesis is sexually dimorphic. Testosterone and estrogen regulate thermogenesis in a sex-specific manner, whereby testosterone reduces thermogenesis in males and estrogen increases thermogenesis in females. Furthermore, animals with high cortisol responsivity to synacthen (HR) have greater susceptibility to obesity than those with low responsivity (LR) and this is due to innate difference in skeletal muscle thermogenesis.