ATTENUATION OF LEPTIN-MEDIATED EFFECTS BY MONOSODIUM GLUTAMATE-INDUCED ARCUATE NUCLEUS DAMAGE

Leptin is a protein secreted by adipocytes that is important in regula ting appetite and adiposity. Recent studies have suggested the presenc e of leptin receptors in the arcuate nucleus of the hypothalamus (ANH) . Neonatal administration of monosodium glutamate (MSG) damages the AN H, resulting in obesity and neuroendocrine dysfunction. Neonatal admin istration of MSG was utilized to test the hypothesis that the anatomic site for many of leptin's actions is the ANH. Female control (n = 6) and MSG-treated rats (n = 7) were implanted for 14 days with osmotic m inipumps containing phosphate-buffered saline or leptin(1 mg.kg(-1).da y(-1)). Leptin suppressed (P < 0.05) body weight gain in controls but did not suppress a-eight gain in MSG-treated rats. Leptin decreased (P < 0.05) fat depots in controls but had no effect in MSG-treated rats. Night feeding was suppressed (P < 0.05) in leptin-treated control rat s. MSG-treated rats showed a suppression in food intake that was of a smaller magnitude and appeared later in the course of leptin treatment . These findings suggest that leptin mediates some physiological actio ns related to fat mobilization via receptors located in the ANH.