Thermogenesis is the dissipation of energy through specialised heat production and contributes to around 15% of total energy expenditure in lean individuals. We developed a model in sheep where food is available at a set meal time (1100-1600h) and we have shown that this establishes a post-prandial induction of thermogenesis in fat and muscle. We sought to characterise post-prandial thermogenesis in two models of obesity. Firstly, we manipulated adiposity through diet. Diet-induced obesity did not alter thermogenesis in adipose tissue or skeletal muscle compared to control animals. On the other hand, chronic food restriction reduced the expression of UCP3 in skeletal muscle and this coincided with lowered muscle temperature. With regard to adipose tissue, thermogenesis was primarily impaired in the sternal depot of lean animals compared to control and obese groups. Thus, reduced thermogenesis in both adipose tissue and skeletal muscle is a compensatory mechanism to preserve body weight under chronic food restriction.
In addition to diet-induced obesity we measured thermogenesis in genetically lean and obese sheep. Genetically lean and obese animals have been selectively bred across 15 generations. The physiological mechanisms underpinning differences in body composition, however, remain to be elucidated since food intake is similar between the two groups. We demonstrate that post-prandial thermogenesis is lower in adipose tissue of the obese animals. This difference is specific to adipose thermogenesis as skeletal muscle temperature was similar between obese and lean animals. Thus, innate differences in adipose thermogenesis may underpin differences in body composition in lean and obese animals.
Overall we have demonstrated that changes in thermogenesis occur in response to food restriction in line with adaptive responses to maintain energy homeostasis. In addition, innate differences in thermogenesis may underlie altered propensity to obesity.