Wapnir R A
Department of Pediatrics, North Shore Long Island Jewish Health System and New York University School of Medicine, Manhasset, NY 11030, USA.
J Nutr. 2000 May;130(5S Suppl):1388S-92S. doi: 10.1093/jn/130.5.1388S.
Recent clinical and experimental findings have reinforced the link among zinc deficiency, malnutrition and diarrheal disease. Because there is a strong association between protein and zinc content in virtually all types of foods, insufficient protein intake may often be the cause of zinc deficiency. Compensatory mechanisms operating in monogastric species during malnutrition are less effective for the absorption of transition divalent elements such as zinc, which remain bound to ligands of dietary or endogenous origin. Both protein and zinc deficiencies are strong negative determinants for normal cellular immunity. In zinc deficiency, the organism is more susceptible to toxin-producing bacteria or enteroviral pathogens that activate guanylate and adenylate cyclases, stimulating chloride secretion, producing diarrhea and diminishing absorption of nutrients, thus exacerbating an already compromised mineral status. In addition, zinc deficiency may impair the absorption of water and electrolytes, delaying the termination of normally self-limiting gastrointestinal disease episodes. The gastrointestinal tract may be one of the first target areas where zinc insufficiency may be manifested. A prolonged low zinc intake deprives the organism of the local potential beneficial effects of zinc, including interactions with oxidative free radicals and nitric oxide metabolism. Nitric oxide is a second messenger that plays an important part in the triggering of diarrheal disease. The possible interrelationship among infection, inflammation, free radical damage and its quenching by potential scavengers, such as zinc, in the intestinal lumen or within the enterocyte should be more extensively studied.
近期的临床和实验研究结果进一步证实了锌缺乏、营养不良与腹泻病之间的联系。由于几乎所有类型食物中的蛋白质和锌含量之间存在紧密关联，蛋白质摄入不足往往可能是锌缺乏的原因。在营养不良期间，单胃动物体内的代偿机制对锌等二价过渡元素的吸收效果较差，这些元素仍与膳食或内源性配体结合。蛋白质和锌缺乏都是正常细胞免疫的强烈负面决定因素。在锌缺乏时，机体更容易受到产生毒素的细菌或肠道病毒病原体的侵袭，这些病原体激活鸟苷酸环化酶和腺苷酸环化酶，刺激氯离子分泌，导致腹泻并减少营养物质的吸收，从而加剧原本就已受损的矿物质状况。此外，锌缺乏可能会损害水和电解质的吸收，延迟通常自限性胃肠道疾病发作的终止。胃肠道可能是锌不足最早表现出来的靶器官之一。长期低锌摄入会使机体无法获得锌的局部潜在有益作用，包括与氧化自由基的相互作用以及一氧化氮代谢。一氧化氮是一种第二信使，在腹泻病的引发中起重要作用。感染、炎症、自由基损伤以及锌等潜在清除剂在肠腔或肠细胞内对其淬灭之间可能存在的相互关系，应进行更广泛的研究。
