Essatara M B, Morley J E, Levine A S, Elson M K, Shafer R B, McClain C J
Physiol Behav. 1984 Mar;32(3):475-8. doi: 10.1016/0031-9384(84)90266-x.
Anorexia is a major symptom of zinc deficiency, but the mechanism(s) for this anorexia are poorly defined. Recent studies have suggested an integral role for endogenous opiate peptides in appetite regulation. Dynorphin, a leucine-enkephalin containing opiate peptide, is a potent inducer of spontaneous feeding. In this study we showed that zinc deficient animals were relatively resistant to dynorphin-induced feeding. Measurement of dynorphin levels using a highly sensitive radioimmunoassay showed that zinc deficient animals had lower levels of dynorphin in the hypothalamus than did ad lib fed animals, with weight restricted animals having intermediate values. [3H]-naloxone binding was significantly increased to isolated brain membranes from zinc deficient animals using 1 nM unlabeled naloxone when compared to ad lib fed controls with the weight restricted animals again having intermediate values. These data suggest that abnormalities in endogenous opiate regulation of appetite may well play a role in the anorexia of zinc deficiency. The effects of zinc deficiency on endogenous opiate action appear to include alterations in receptor affinity, a post-receptor defect and alterations in the synthesis and/or release of dynorphin.
厌食是锌缺乏的主要症状，但这种厌食的机制尚未明确。最近的研究表明内源性阿片肽在食欲调节中起重要作用。强啡肽是一种含亮氨酸脑啡肽的阿片肽，是自发进食的有效诱导剂。在本研究中，我们发现缺锌动物对强啡肽诱导的进食相对抵抗。使用高灵敏度放射免疫测定法测量强啡肽水平，结果显示缺锌动物下丘脑的强啡肽水平低于自由采食动物，限食动物的强啡肽水平介于二者之间。与自由采食对照相比，使用1 nM未标记的纳洛酮时，缺锌动物分离的脑膜上的[3H] - 纳洛酮结合显著增加，限食动物的结合量再次介于二者之间。这些数据表明内源性阿片肽对食欲的调节异常可能在锌缺乏引起的厌食中起作用。锌缺乏对内源性阿片肽作用的影响似乎包括受体亲和力改变、受体后缺陷以及强啡肽合成和/或释放的改变。
