Publisher Summary A reduced energy expenditure on non-shivering thermogenesis (NST) has been established as a primary cause of obesity in the genetically obese (ob/ob) and diabetic–obese (db/db) strains of mice. In newborn mammals and in hibernators, the brown adipose tissue (BAT) is the main site of NST, and Foster and Frydman have recently shown that this is also true for cold-exposed adult rodents. The presence of similar thermoregulatory abnormalities in ob/ob and db/db mice suggests that these two mutants may have a common metabolic basis to their obesity. Interscapular BAT, which occurs in two discrete pads between the shoulder blades, is two to three times heavier in the diabetic–obese mutant than in lean mice, and this can be accounted for by elevated lipid content. There are biochemical abnormalities in BAT of the db/db mutant that are similar to those reported for the ob/ob mouse and that are consistent with a reduced energy expenditure on NST.