Prasad A S
Spec Top Endocrinol Metab. 1985;7:45-76.
The requirement of zinc for humans was recognized in the early 1960s. The causes of zinc deficiency include malnutrition, alcoholism, malabsorption, extensive burns, chronic debilitating disorders, and chronic renal diseases; use of certain drugs such as penicillamine and, in some cases, diuretics; and genetic disorders such as acrodermatitis enteropathica and sickle cell disease. The requirement of zinc is increased in pregnancy and during growth. The clinical manifestations of severe zinc deficiency include bullous-pustular dermatitis, alopecia, diarrhea, emotional disorder, weight loss, intercurrent infections, and hypogonadism in males; zinc deficiency can be fatal if unrecognized and untreated. A moderate deficiency of zinc is characterized by growth retardation and delayed puberty in adolescents, hypogonadism in males, rough skin, poor appetite, mental lethargy, delayed wound healing, taste abnormalities, and abnormal dark adaptation. In mild cases of zinc deficiency in human subjects, we have observed oligospermia, slight weight loss, and hyperammonemia. Zinc is a growth factor. As a result of its deficiency, growth is affected adversely in many animal species and humans, probably because zinc is needed for protein and DNA synthesis and cell division. The effects of zinc and growth hormone on growth appear to be independent of each other in experimental animals. Whether zinc is required for the metabolism of somatomedin needs further investigation. Thyroid and adrenal functions do not appear to change as a result of zinc deficiency. Glucocorticoids may have an effect on zinc metabolism, although the clinical relevance of this effect is not known at present. In contrast, testicular function is affected adversely as a result of zinc deficiency in both humans and experimental animals. The effect appears to be a direct one since the hypothalamic-pituitary axis is intact, and may relate to the reduction in testicular size as a result of the need for zinc in cell division. In addition, zinc is required for the function of several testicular enzymes, although a specific role in steroidogenesis has not been identified. Zinc appears to have a role in the modulation of prolactin secretion, in the secretion and action of insulin, and in the production and biologic effects of thymic hormones. It is clear that the endocrine consequences of zinc deficiency are multiple, and that continued investigation should provide additional pathophysiologic and therapeutic insights.
人类对锌的需求在20世纪60年代初得到确认。锌缺乏的原因包括营养不良、酗酒、吸收不良、大面积烧伤、慢性消耗性疾病和慢性肾脏疾病；使用某些药物如青霉胺，在某些情况下还有利尿剂；以及遗传性疾病如肠病性肢端皮炎和镰状细胞病。孕期和生长期间锌的需求量会增加。严重锌缺乏的临床表现包括大疱性脓疱性皮炎、脱发、腹泻、情绪紊乱、体重减轻、并发感染以及男性性腺功能减退；如果未被识别和治疗，锌缺乏可能是致命的。中度锌缺乏的特征是青少年生长发育迟缓、青春期延迟、男性性腺功能减退、皮肤粗糙、食欲不佳、精神萎靡、伤口愈合延迟、味觉异常以及暗适应异常。在人类轻度锌缺乏病例中，我们观察到少精子症、轻微体重减轻和高氨血症。锌是一种生长因子。由于锌缺乏，许多动物物种和人类的生长都会受到不利影响，这可能是因为蛋白质和DNA合成以及细胞分裂都需要锌。在实验动物中，锌和生长激素对生长的影响似乎是相互独立的。锌是否是生长调节素代谢所必需的，还需要进一步研究。甲状腺和肾上腺功能似乎不会因锌缺乏而改变。糖皮质激素可能对锌代谢有影响，尽管目前这种影响的临床相关性尚不清楚。相比之下，人类和实验动物的锌缺乏都会对睾丸功能产生不利影响。这种影响似乎是直接的，因为下丘脑 - 垂体轴是完整的，可能与细胞分裂需要锌导致睾丸大小减小有关。此外，几种睾丸酶的功能需要锌，尽管尚未确定其在类固醇生成中的具体作用。锌似乎在调节催乳素分泌、胰岛素的分泌和作用以及胸腺激素的产生和生物学效应中发挥作用。显然，锌缺乏的内分泌后果是多方面的，持续的研究应该会提供更多的病理生理学和治疗方面的见解。
