Dawson R, Pelleymounter M A, Millard W J, Liu S, Eppler B
Department of Pharmacodynamics, College of Pharmacy, University of Florida, Gainesville 32610, USA.
Am J Physiol. 1997 Jul;273(1 Pt 1):E202-6. doi: 10.1152/ajpendo.1997.273.1.E202.
Leptin is a protein secreted by adipocytes that is important in regulating appetite and adiposity. Recent studies have suggested the presence of leptin receptors in the arcuate nucleus of the hypothalamus (ANH). Neonatal administration of monosodium glutamate (MSG) damages the ANH, resulting in obesity and neuroendocrine dysfunction. Neonatal administration 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 minipumps containing phosphate-buffered saline or leptin (1 mg.kg-1.day-1). Leptin suppressed (P < 0.05) body weight gain in controls but did not suppress weight 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 rats. 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 actions related to fat mobilization via receptors located in the ANH.
瘦素是一种由脂肪细胞分泌的蛋白质，在调节食欲和肥胖方面具有重要作用。最近的研究表明，下丘脑弓状核（ANH）中存在瘦素受体。新生期给予谷氨酸单钠（MSG）会损害ANH，导致肥胖和神经内分泌功能障碍。利用新生期给予MSG来检验瘦素许多作用的解剖部位是ANH这一假说。将雌性对照大鼠（n = 6）和经MSG处理的大鼠（n = 7）植入含有磷酸盐缓冲盐水或瘦素（1 mg·kg⁻¹·天⁻¹）的渗透微型泵，持续14天。瘦素抑制（P < 0.05）对照大鼠的体重增加，但对经MSG处理的大鼠体重增加没有抑制作用。瘦素减少（P < 0.05）对照大鼠的脂肪储存，但对经MSG处理的大鼠没有影响。经瘦素处理的对照大鼠的夜间进食受到抑制（P < 0.05）。经MSG处理的大鼠在瘦素治疗过程中食物摄入量的抑制程度较小且出现较晚。这些发现表明，瘦素通过位于ANH中的受体介导一些与脂肪动员相关的生理作用。
