Brown adipose tissue (BAT) in mammals performs non-shivering thermogenesis. This function is mainly thought to be carried out by uncoupling protein 1(UCP1), an inner mitochondrial membrane protein that dissipates proton gradient as heat. Active BAT in humans correlates with improved metabolic health. Thus, there is interest in therapeutically stimulating BAT to combat obesity. A conventional view is that active BAT catabolizes glucose and fatty acids to fuel the tricarboxylic acid (TCA) cycle, which provides the electron donors to drive the mitochondrial membrane potential and UCP1-mediated uncoupling. However, during cold exposure, the TCA intermediate citrate is exported from the mitochondria into the cytosol, where it is converted to acetyl- CoA, which fuels de novo lipid synthesis. A portion of these lipids are then immediately catabolized through beta-oxidation, resulting in simultaneous fatty acid synthesis (FAS) and fatty acid oxidation (FAO). Why this paradox occurs during thermogenesis has long been a mystery. To test this, we generated several brown fat-specific knockout models in the de novo lipid synthesis pathway. Using these models, we have shown that SLC25A1, mitochondrial citrate carrier, and ATP citrate lyase (ACLY), the enzyme that cleaves citrate into acetyl-CoA, are essential for mitochondrial/thermogenic program in the brown fat, and they allow citrate exit from mitochondria and thus mitigate mitochondrial stress under carbohydrate-rich conditions. Overall, we propose a model in which FAS-FAO cycling is crucial and can relieve mitochondrial stress, generate important metabolites for thermogenesis, contribute to heat production through multiple ATP hydrolysis steps, and dissipate energy excess, which can be utilized therapeutically.