Neuropharmacology of obesity: my receptors made me eat it.

β3-Adrenergic Receptors The 3 distinct subtypes of β receptors are the β1 receptor, which is predominantly a cardiac receptor and the target for β blockers; β2 receptor, which is in the lungs (the target of bronchodilating β agonists) and also found in uterus and skeletal muscle; and β3 receptor, expressed primarily in adipose tissue, where it regulates energy metabolism and thermogenesis (turning fat into heat and energy), especially in response to norepinephrine. Evidence that the β3-adrenergic receptors play an active role in weight control in humans comes from the finding that a genetic variant of this receptor constitutes a susceptibility factor for the onset of morbid obesity as well as non-insulin-dependent diabetes. Specifically, this variant of the β3 receptor is associated with hereditary obesity in Pima Indians from Arizona and demonstrated an increased incidence in obese patients in Japan. It also exists in nonobese individuals, including a fourth of African Americans and BRAINSTORMS is a monthly section of The Journal of Clinical Psychiatry aimed at providing updates of novel concepts emerging from the neurosciences that have relevance to the practicing psychiatrist. From the Clinical Neuroscience Research Center in San Diego and the Department of Psychiatry at the University of California San Diego. Reprint requests to: Stephen M. Stahl, M.D., Ph.D., Editor, BRAINSTORMS, 8899 University Center Lane, Suite 130, San Diego, CA 92122. ody weight is regulated by complex interrelationships between central and peripheral factors. Satiety, appetite, and craving are CNS drives, whereas metabolism and energy utilization are peripheral endocrine actions. Recent discoveries are lending important insights into how these central and peripheral components of weight control are mediated by receptors for several key neurotransmitters and hormones. Since obesity results from an imbalance between caloric intake and energy expenditure, these new findings suggest that treatment of obesity can be based both on central mechanisms that decrease the urge to eat and on peripheral mechanisms that increase the mobilization of energy.