The large capacity of brown adipose tissue (BAT) to expend energy as heat makes it an interesting potential player in weight regulation and other metabolic conditions. This is of particular interest as it has been recognized that adult humans possess BAT. The protein responsible for the heat production is uncoupling protein 1 (UCP1), which, as the name implies, uncouples the respiratory chain from ATP production; instead heat is produced. Cold is the strongest recruiter and activator of BAT. However, also obesogenic food has a low but nonetheless significant effect on the recruitment and activation of UCP1, although the significance of this has been discussed.

In the present thesis, I have studied the effect of diet on BAT and the possibilities for it to be obesity-protective. This can be done by comparing responses in wild-type mice and in UCP1-ablated mice. Since the effect of diet on BAT is low, it is of importance to control the temperature and maintain thermoneutrality. Other confounding factors to keep in mind are differences in actual energy and composition of food and also cohort differences. When controlling all the parameters mentioned and giving the mice the same obesogenic diet, the mice possessing UCP1 compared to UCP1-ablated mice had higher energy expenditure, and lower weight gain, despite eating more. This confirms the presence of a UCP1-dependent diet-induced thermogenesis. Thus, the conclusion must be that possessing UCP1 does result in obesity protection at thermoneutrality. However, the relevance for human energy balance is still not established.