The Koletsky (“corpulent”) obese rat is homozygous for an autosomal recessive mutation of the leptin receptor (Lepr) that results in hyperphagia, obesity, and hyperlipidemia. Unlike the Lepr mutation that characterizes thefatty Zucker rat (Lepr ^fa ), the Koletsky mutation (Lepr ^fak ) is null. Because the Lepr^fak mutation is null, exogenous leptin should have no effect on body weight or food intake infa^k/fa ^k rats. We confirmed that prediction: murine leptin, administered into the third ventricle for 5 consecutive days, did not affect daily food intake or body weight infa^k/fa ^k rats but produced dose-related inhibitions of food intake and body weight in+/+ and +/fa ^k rats. Althoughfa^k/fa ^k rats did not respond to leptin, their response to CCK-8 (4 μg/kg ip) injected before 30-min test meals of 10% sucrose was not different from that of +/+ or+/fa^k rats. These results demonstrate that thefa^k/fa ^k rat is a good model in which to analyze the controls of food intake, energy expenditure, and energy storage in the absence of leptin effects.