Kalra S P, Xu B, Dube M G, Moldawer L L, Martin D, Kalra P S
Department of Neuroscience, University of Florida College of Medicine, Gainesville 32610, USA.
Neurosci Lett. 1998 Jan 2;240(1):45-9. doi: 10.1016/s0304-3940(97)00896-3.
Periods of chronic undernutrition and short periods of fasting suppress pituitary luteinizing hormone (LH) secretion and upregulate hypothalamic neuropeptide Y (NPY), the orexigenic peptide. The effect of suppression of NPY upregulation with ciliary neurotropic factor (CNTF), a cytokine, and leptin, an adipocyte hormone, on pituitary LH secretion was evaluated in fasted rats. In the first experiment, daily injection of CNTF (0.2 nmol) intracerebroventricularly (i.c.v.) for 4 days drastically reduced food intake and body weight gain similar to the weight loss seen in pair-fed rats. Food deprivation (FD) also decreased body weight. Despite drastic loss in body weight, plasma LH was reduced in FD and pair-fed rats, but not in CNTF-treated rats. In the second experiment, FD rats received either control vehicle, CNTF (0.2 nmol) or leptin (0.2 nmol) daily for 4 days. FD increased steady state levels of preproNPY mRNA in the hypothalamus over the control freely-fed rats. However, both CNTF and leptin suppressed hypothalamic gene expression and significantly attenuated LH suppression in response to FD. Taken together, these results support the hypothesis that the upregulation of hypothalamic NPY system may underlie diminution in pituitary gonadotropin secretion and that the NPYergic pathway may serve as a communication bridge between the neural processes that regulate reproduction and those that maintain energy balance.
长期营养不良和短期禁食会抑制垂体促黄体生成素（LH）的分泌，并上调下丘脑促食欲肽神经肽Y（NPY）。在禁食大鼠中评估了细胞因子睫状神经营养因子（CNTF）和脂肪细胞激素瘦素对NPY上调的抑制作用对垂体LH分泌的影响。在第一个实验中，连续4天每天脑室内注射（i.c.v.）CNTF（0.2 nmol），食物摄入量和体重增加大幅减少，类似于配对喂养大鼠的体重减轻。食物剥夺（FD）也会降低体重。尽管体重急剧下降，但FD组和配对喂养大鼠的血浆LH降低，而CNTF处理的大鼠则没有。在第二个实验中，FD大鼠连续4天每天接受对照载体、CNTF（0.2 nmol）或瘦素（0.2 nmol）。与自由进食的对照大鼠相比，FD增加了下丘脑前NPY原mRNA的稳态水平。然而，CNTF和瘦素均抑制下丘脑基因表达，并显著减弱FD引起的LH抑制。综上所述，这些结果支持以下假设：下丘脑NPY系统的上调可能是垂体促性腺激素分泌减少的基础，并且NPY能途径可能作为调节生殖的神经过程与维持能量平衡的神经过程之间的通讯桥梁。
