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Physiological Regulation of Appetite

Acute insulin-induced elevations of circulating leptin and feeding inhibition in lean but not obese rats

¹Department of Biomedical Engineering, Columbia University, New York, and ²Obesity Research Center, Department of Medicine, St. Luke's-Roosevelt Hospital, Columbia University College of Physicians and Surgeons, New York, New York

Submitted 1 November 2004 ; accepted in final form 16 March 2005

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-mo-old female selectively bred obesity-resistant (OR) and obesity-prone (OP) Sprague-Dawley rats maintained on laboratory chow to investigate this question. At testing, body weights and basal leptin levels of the OP rats were significantly elevated compared with the OR rats. In the 3-h fasted state, injection of 2.0 U insulin/kg ip resulted in significant elevations of plasma leptin at 4 h postinjection in both OP and OR groups (hour 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 hours 2–4 after 2.0 U/kg of insulin in the OR (–80.1%, P < 0.05), but not in the OP group, compared with intake after saline injections. In feeding tests with palatable moderately high-fat pellets after 2.0 and 3.0 U insulin/kg ip, significant decreases between hours 2 and 4 in 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 feeding-related insulin release.

hyperphagia; leptin resistance; obese animal model; diet palatability; satiety

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