In rodent models of chronic and unremitting sleep deprivation, hyperphagia develops after 5‐6 days. If the regimen is taken to 10‐20 days, food intake increases substantially irrespective of whether rats are fed chow or a palatable calorie‐dense liquid diet (Ensure); body weight does not increase. Moreover, in a new model of chronic sleep restriction, sleep deprivation is enforced for 20 hours followed by 4 hours of recovery in home cages, and this also leads to hyperphagia. Of importance is that despite greatly increased food intake in all paradigms, rats consistently fail to gain body weight. This can only happen if there is an increase in energy metabolism. Indeed, the resting metabolic rate of sleep‐deprived rats becomes elevated, mediated by robust up‐regulation of uncoupling protein 1 in brown adipose tissue. Additionally, gene expression of uncoupling protein 3 in skeletal muscle is strongly stimulated, although the role of this protein in thermogenesis remains controversial. Chronically sleep‐deprived rats show rapid mobilization of hepatic and muscle glycogen, followed by reduction in abdominal white adipose tissue. Despite a lack of weight gain, there is evidence to suggest that sleep deprivation/restriction leads to glucose dysregulation. For example, sleep‐deprived rats have a higher glucose:insulin ratio, and when challenged with an intraperitoneal glucose tolerance test, blood glucose of sleep‐restricted rats is higher than in controls. In summary, rat models of sleep deprivation/restriction may be useful tools in understanding the etiology of hyperphagia and suggest a dissociation between weight gain and glucose dysregulation and insulin resistance.Supported by NCRR RCMI and a Pilot and Feasibility grant from the Clinical Nutrition Research Unit of Maryland, P30DK072488.