Obesity is a global problem and effective drug therapy treatment is still unavailable. Obesity develops due to an imbalance between energy intake and energy expenditure (EE). Understanding what happens to EE in obesity may be the key to developing new treatments for obesity. If EE in obesity can be elevated, it could be a potential therapeutic target. We recently discovered that in baseline conditions obese mice have increased EE, in terms of thermogenesis. However, this increase in EE is not great enough to offset the elevated calorie intake that leads to the development of obesity. In obesity, the adipose derived hormone leptin is significantly elevated. This elevated leptin concentration appears to cause an increase in thermogenesis through increased sympathetic nerve activity (SNA) to brown adipose tissue deposits. The brain region of the dorsomedial hypothalamus (DMH) appears to be a key region that leptin activates in obesity to cause this increased thermogenesis. One unsettling finding is that the sympathetic nervous system (SNS) in obesity is elevated via leptin and it seems unlikely that SNA would be selectivity increased to only brown adipose tissue. Previously, it has been observed that leptin can increase SNA to numerous organs including the kidney. Furthermore, in obesity, SNA is increased in numerous organs. This leads to the critical question: is the leptin-mediated elevation of SNA and thermogenesis also chronically activating the kidney and contributing to the development of hypertension in obesity?