Lee R G, Rains T M, Tovar-Palacio C, Beverly J L, Shay N F
Division of Nutritional Sciences, Department of Food Science and Human Nutrition, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
J Nutr. 1998 Jul;128(7):1218-23. doi: 10.1093/jn/128.7.1218.
Zinc deficiency reduces intake and produces an unusual approximately 3.5-d cycle of intake in rats. The mechanism underlying the anorexia and cycling has not yet been defined; current hypotheses suggest that alterations in amino acid metabolism and neurotransmitter concentrations may be a part of this anorexia. Recent reports indicate that appetite-stimulating neuropeptide Y (NPY) may be elevated during zinc deficiency. This suggests that a resistance to NPY may exist during zinc deficiency because NPY levels are high, yet appetite is low. The purpose of this study was to measure NPY peptide and mRNA concentrations during zinc deficiency in specific nuclei of the hypothalamus in which peptide and mRNA for NPY are known to be associated with appetite, and also to determine whether zinc-deficient rats are responsive to central infusions of NPY. Both NPY peptide levels in the paraventricular nucleus and NPY mRNA levels in the arcuate nucleus were higher (P < 0.05) in zinc-deficient rats than in zinc-adequate rats. When rats were administered exogenous NPY to the paraventricular nucleus, both zinc-deficient and zinc-adequate rats responded similarly by increasing food intake. These results suggest that NPY is elevated during zinc deficiency in an attempt to restore normal food intake levels, rather than being reduced and thereby contributing to the anorexia associated with zinc deficiency. During zinc deficiency, NPY receptors are able to bind NPY and initiate an orexigenic response.
锌缺乏会减少大鼠的食物摄入量，并产生一个约3.5天的异常进食周期。厌食和进食周期背后的机制尚未明确；目前的假说认为氨基酸代谢和神经递质浓度的改变可能是这种厌食的一部分。最近的报告表明，在锌缺乏期间，刺激食欲的神经肽Y（NPY）可能会升高。这表明在锌缺乏期间可能存在对NPY的抵抗，因为NPY水平很高，但食欲却很低。本研究的目的是测量锌缺乏期间下丘脑特定核团中NPY肽和mRNA的浓度，已知这些核团中的NPY肽和mRNA与食欲有关，同时确定缺锌大鼠对中枢注射NPY是否有反应。缺锌大鼠室旁核中的NPY肽水平和弓状核中的NPY mRNA水平均高于锌充足的大鼠（P < 0.05）。当向大鼠室旁核注射外源性NPY时，缺锌和锌充足的大鼠的反应相似，均通过增加食物摄入量来响应。这些结果表明，在锌缺乏期间NPY升高是为了试图恢复正常的食物摄入量，而不是降低从而导致与锌缺乏相关的厌食。在锌缺乏期间，NPY受体能够结合NPY并引发促食欲反应。
