Activation of brown fat and browning of white fat by cold exposure or beta 3 adrenergic receptor agonists increases energy expenditure and ameliorates metabolic syndrome. However, cold exposure or beta 3 adrenergic receptor agonists induced thermogenesis has achieved limited clinical efficacy, and alternative measures need to be explored to stimulate brown fat and white fat browning. Here we reveal a critical role of sodium chloride in promoting activity of brown fat and browning of white fat. Our study found that 2% salt in drinking water significantly increases energy expenditure (EE) of wild type mice via the activation of BAT activity and WAT browning, as evidenced by the upregulation of UCP1 and PGC-1α at mRNA and protein level in both brown fat and inguinal white fat. Moreover, salt intake significantly increases body temperature without a change in food intake and locomotive activity, leading to a marked decrease in fat mass as well as diet-induced obesity. Mechanistically, salt intake decreases hypothalamic Arc NPY expression, leading to the removal of inhibition on tyrosine hydroxylase (TH) activity in the hypothalamic PVN, thereby resulting in increased sympathetic outflow to peripheral BAT and WATi. Taken together, these data suggest that salt ingestion stimulates the activity of brown fat and browning of white fat and enhances energy expenditure through the modulation of central hypothalamic NPY-TH levels. The results from this study for the first time reveal the novel role of salt intake in controlling thermogenesis. The findings will provide insights into using salt as an alternative treatment option for high fat induced metabolic disorders.