Zinc as an appetite stimulator - the possible role of zinc in the progression of diseases such as cachexia and sarcopenia.
Zinc as an appetite stimulator - the possible role of zinc in the progression of diseases such as cachexia and sarcopenia.
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DOI：
10.2174/2212798411103030226
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发表时间：
2011-08
影响因子：
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通讯作者：
Hajime Suzuki;A. Asakawa;J. Li;M. Tsai;Haruka Amitani;Kousaku Ohinata;M. Komai;A. Inui
中科院分区：
文献类型：
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作者：
Hajime Suzuki;A. Asakawa;J. Li;M. Tsai;Haruka Amitani;Kousaku Ohinata;M. Komai;A. Inui
锌是人类和动物所必需的许多生理功能，如生长，免疫功能和生殖。锌缺乏会引起许多生理问题，包括厌食、生长迟缓、皮炎、味觉障碍和性腺功能减退。虽然缺锌在实验动物中产生特异性和严重的厌食症是很清楚的，但缺锌和厌食症之间的联系还不太确定。我们是第一个表明，口服，但不是腹腔注射，锌迅速刺激食物摄入，通过食欲肽耦合到传入迷走神经使用大鼠在早期缺锌，而不降低锌浓度的血浆和组织。我们证实，锌充足的饮食含有氯化锌急性刺激食物摄入后，短期锌剥夺。我们还发现，口服硫酸锌后，NPY和食欲素mRNA的表达增加。使用迷走神经切断的大鼠，我们测试了口服锌后食物摄入量的增加是否由迷走神经介导。在假手术大鼠中，口服锌刺激食物摄入，而锌和生理盐水给药在迷走神经切断大鼠中没有表现出不同的影响。我们的结论是，锌刺激短期缺锌大鼠通过传入迷走神经与随后的影响下丘脑肽与食物摄入调节的食物摄入。本文综述了锌作为食欲刺激剂在食物摄入调节中的作用，沿着下丘脑、ghrelin、leptin和锌受体的研究，以及锌在神经性厌食、恶病质和肌肉减少症中的临床应用。文章还介绍了一些有前途的锌专利。
Zinc is required by humans and animals for many physiological functions, such as growth, immune function, and reproduction. Zinc deficiency induces a number of physiological problems, including anorexia, growth retardation, dermatitis, taste disorder, and hypogonadism. Although it is clear that zinc deficiency produces specific and profound anorexia in experimental animals, the connection between zinc deficiency and anorexia is less certain. We were the first to show that orally, but not intraperitoneally, administered zinc rapidly stimulates food intake through orexigenic peptides coupled to the afferent vagus nerve using rats during early-stage zinc deficiency without decreased zinc concentrations in plasma and tissues. We confirmed that a zinc-sufficient diet containing zinc chloride acutely stimulated food intake after short-term zinc deprivation. We also found that orally administered zinc sulfate increased the expression of NPY and orexin mRNA after administration. Using vagotomized rats, we tested whether the increase in food intake after oral administration of zinc was mediated by the vagus nerve. In sham-operated rats, the oral administration of zinc stimulated food intake, whereas zinc and saline administrations did not exhibit differing effects in vagotomized rats. We conclude that zinc stimulates food intake in short-term zinc-deficient rats through the afferent vagus nerve with subsequent effects on hypothalamic peptides associated with food intake regulation. In this review, we describe recent research investigating the roles of zinc as an appetite stimulator in food intake regulation, along with research about hypothalamus, ghrelin, leptin and zinc receptor, and clinical application about anorexia nervosa, cachexia and sarcopenia. The article also presents some promising patents on zinc.