Insulin has been shown to stimulate leptin mRNA expression acutely in rat adipose tissue, but its short-term effects on circulating leptin levels, and subsequent feeding behavior, have not been well described. We used 11-month old female selectively bred obesityresistant (OR) and obesity-prone (OP) Sprague-Dawley groups maintained on laboratory chow to investigate this question. At testing, body weights and basal leptin levels of the OP rats were significantly elevated in comparison with OR rats. In the 3-hr fasted state, injection of 2.0 U insulin/Kg i.p. resulted in significant elevations of plasma leptin at 4 hr post-injection in both OP and OR groups (hr 4, +2.50 and +5.98 ng/ml, respectively). In separate feeding tests with the same groups, intake of laboratory chow pellets was significantly inhibited during hr 2-4 following 2.0U/kg of insulin in the OR (-80.1%, p<0.05), but not in the OP group, in comparison with intake following saline injections. In feeding tests with palatable moderately high fat pellets following 2.0 and 3.0 U insulin/Kg i.p., significant decreases of hr 2-4 intake were seen in the OR group only (-41.0 and -68.3%, respectively). Thus, feeding inhibition coincides with insulin-induced elevations of plasma leptin in lean, but not obese Sprague-Dawley rats. Our data suggest that elevations of leptin within the physiological range may contribute to short-term inhibition of food intake in rats, and that this process may be stimulated by feedingrelated insulin release.