Recently, important insights were gained into the control of food intake and energy expenditure by the newly discovered adipocyte-derived hormone OB (the ob gene product, dubbed leptin) as well as into the pathogenetic role of the adipocyte-specific β3-adrenergic receptor, mutations of which predispose to obesity, insulin resistance and early onset of non-insulin dependent diabetes mellitus. The latter studies are the topic of the second part of this month's Highlights section.
The genetically obese mouse strain (ob/ob) suffering from type II diabetes and hypothermia was described over 40 years ago. Early studies elegantly demonstrated the absence of a defect in a circulating factor in these mice, since parabiosis experiments (coupling of the circulatory systems) of an ob/ob mouse with a normal partner induced weight loss and a decrease in food intake in the ob/ob mouse. Similarly, joining two normal mice by parabiosis and