Women typically possess more adipose tissue than men, but they are relatively protected against developing cardiometabolic diseases, including cardiovascular disease and type 2 diabetes. Across the menopausal transition, women tend to gain weight and become susceptible to metabolic and cardiovascular diseases. Such weight gain and loss of cardiometabolic protection is due, at least in part, to declining levels of estrogen. Body weight is determined by energy intake and energy expenditure, wherein total energy expenditure is determined by basal metabolic rate, physical activity and adaptive thermogenesis. Adaptive thermogenesis refers to the dissipation of energy through cellular heat production and occurs in mitochondrial enriched tissues, such as brown adipose tissue (BAT). Numerous animal studies have demonstrated that estrogen acts within the brain to regulate both reproductive and metabolic functions. Regarding the latter, estrogen acts on neurons in the hypothalamus to reduce food intake and to increase energy expenditure. In particular, estrogen acts to increase thermogenesis. Despite this, little is known of how sex steroids modulate thermogenesis in healthy adults. This symposium presentation will explain sexual dimorphism in relation to thermogenesis and will examine the role of sex steroids in the regulation of the same in healthy young men and women. I will highlight a possible role for brown adipose tissue in conferring protection against cardiometabolic disease in women.