The hormone sensitive lipase (HSL) catalyzes the final, rate limiting step of energy mobilization from adipose tissue. Its activation results in hydrolysis of triglycerides, a process referred to as lipolysis. Increased HSL activity during fasting and stress, is physiologically coupled with significant reductions in circulating leptin levels, which in turn, results in increased food intake, and thus, restoration of energy balance. We hypothesize that local neural signals from the sympathetic nervous system to adipocytes through beta-adrenergic receptors simultaneously regulate leptin secretion and lipolysis, the latter via the modulation of HSL activity. This hypothesis will be tested by measurements of interstitial levels of leptin and glycerol in adipose tissue in situ before and after local administration of a beta-adrenergic agonist. Food intake and beta-adrenergic stimulation are excellent potential stimuli in the study of the novel fat-derived hormones, resistin and adiponectin.