to occupy distinct anatomical sites in the body. However, previous work, mainly from our lab, supports the notion that WAT and BAT are in fact found together in subcutaneous and visceral fat depots, collectively forming a multidepot organ that we have called the "adipose organ" ( 4,5 ). This fi nding has opened new perspectives in the physiological relationship between BAT and WAT, including the possibility of their reciprocal transformation (transdifferentiation) ( 6-8 ). Harnessing the mechanism of WAT to BAT transdifferentiation could be useful to develop treatments for obesity and type 2 diabetes, because the absence of BAT or its †adrenergic receptors results in obesity ( 9, 10 ) and transgenic mice overexpressing UCP1 in WAT are obesity resistant ( 11 ). Furthermore, treatment of obese rodents with †3 agonists increases BAT and curbs obesity ( 12, 13 ). Recently, metabolically active BAT has been described in adult humans. Of note, these subjects have a lower body mass index (BMI) and less visceral fat than those without detectable . C57BL/6J mice are obesity-and type 2 diabetes-prone ( 21 ). In fact, earlier work has shown that C57BL/6J mice are more predisposed to store fat in response to a high-fat diet and to develop obesity, hyperglycemia, and hyperinsulinemia than their obesity-resistant A/J counterparts ( 22 ). Furthermore, it has been suggested that the obesity and diabetes resistance of A/J mice may be due to a strong increase in brown adipocytes in some "classic" white adipose depots after cold exposure or treatment with a †3 adrenergic agonist ( 23, 24 ). Also, a previous work by our group showed that intermuscular fat in the hind legs of C57BL/6J mice contains fewer brown adipocytes than the intermuscular fat of obesity-resistant Sv129 mice (substrain 129/SVPAS SPF/VAF), suggesting the possibility that a difference in BAT amount could explain the susceptibility to obesity and type 2 diabetes of C57BL/6J Abstract White and brown adipocytes are believed to occupy different sites in the body. We studied the anatomical features and quantitative histology of the fat depots in obesity and type 2 diabetes-prone C57BL/6J mice acclimated to warm or cold temperatures. Most of the fat tissue was contained in depots with discrete anatomical features, and most depots contained both white and brown adipocytes. Quantitative analysis showed that cold acclimation induced an increase in brown adipocytes and an almost equal reduction in white adipocytes; however, there were no signifi cant differences in total adipocyte count or any signs of apoptosis or mitosis, in line with the hypothesis of the direct transformation of white into brown adipocytes. The brown adipocyte increase was accompanied by enhanced density of noradrenergic parenchymal nerve fi bers, with a signifi cant correlation between the density of these fi bers and the number of brown adipocytes. Comparison with data from obesity-resistant Sv129 mice disclosed a signifi cantly different brown adipocyte content in C57BL/6J mice, suggesting that th...