In a world where food availability is intermittent, survival requires the capacity to store ingested calories in excess of immediate requirements so that energy may be released at a later point upon demand. To orchestrate these processes of energy storage and release, highly integrated systems have evolved, and these operate on several physiological levels. As for many complex physiologic systems, the brain provides an essential coordinating role. Most important are the hypothalamic centers (see Figure 1) that coordinate energy homeostasis through regulation of food intake (hunger and satiety), energy expenditure (thermogenesis), and the secretion of hormones (especially insulin) that regulate substrate interconversion, storage, and mobilization. But where does the energy storage take place? Enter the adipocyte, and along with it obesity, a remarkably prevalent disorder that is defined as a state of pathologically increased adipose cell mass. Is the adipocyte an innocent bystander, or does it play an active role in the regulation of energy homeostasis and body composition? Although adipose cell enlargement and eventual hypertrophy are the defining features of obesity, the adipocyte has been viewed as a largely passive participant in the disease process, accumulating or losing lipid stores in response to alterations in substrates and regulatory signals produced at distant sites. As a cell type, therefore, the adipocyte has received a great deal of attention only recently, and obesity, the dominant disease affecting adipocyte function, has lacked major breakthroughs in the realm of molecular pathogenesis. Indeed, much of the important research in obesity hastaken place in departments of psychology and psychiatry. Recent advances in the area of adipocyte development and evidence that the adipocyte can function as an endocrine cell have promised to change this situation radically and permanently, and these are the subject of this minireview.