Cátedra de Fisiología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, IQUIMEFA-CONICET, Junín 956, piso 7, Ciudad Autónoma de Buenos Aires, Argentina (1113).
Nutrition. 2011 Apr;27(4):392-8. doi: 10.1016/j.nut.2010.09.010. Epub 2010 Nov 13.
Micronutrient undernutrition during critical periods of growth has become an important health issue in developing and developed countries, particularly among pregnant women and children having an imbalanced diet. Zinc is a widely studied microelement in infant feeding because it is a component of several enzymes involved in intermediary metabolism ranging from growth to cell differentiation and metabolism of proteins, carbohydrates, and lipids. Human and experimental studies have reported an association between zinc deficiency and the etiopathogenesis of cardiovascular and renal diseases like hypertension, atherosclerosis, congestive heart failure, coronary heart disease, and diabetes. The main links between the development of these pathologies and zinc deficiency are multiple mechanisms involving oxidative stress damage, apoptosis, and inflammation. A substantial body of evidence suggests that a poor in utero environment elicited by maternal dietary or placental insufficiency may "programme" susceptibility in the fetus to later development of cardiovascular, renal, metabolic, and endocrine diseases. Zinc deficiency in rats during intrauterine and postnatal growth can also be considered a model of fetal programming of cardiovascular and renal diseases in adult life. Dietary zinc restriction during fetal life, lactation, and/or postweaning induces an increase in arterial blood pressure and impairs renal function in adult life. This review focuses on the contributions of experimental and clinical studies to current knowledge of the physiologic role of zinc in the cardiovascular and renal systems. Moreover, this review examines the relationship between zinc deficiency during different periods of life and the development of cardiovascular and renal diseases in adult life.
在生长关键期发生的微量营养素营养不良已成为发展中国家和发达国家的一个重要健康问题，尤其是在饮食不均衡的孕妇和儿童中。锌是婴儿喂养中广泛研究的微量元素，因为它是参与中间代谢的几种酶的组成部分，从生长到细胞分化以及蛋白质、碳水化合物和脂质的代谢。人体和实验研究报告称，锌缺乏与心血管和肾脏疾病（如高血压、动脉粥样硬化、充血性心力衰竭、冠心病和糖尿病）的病因发病机制之间存在关联。这些病理发展与锌缺乏之间的主要联系是涉及氧化应激损伤、细胞凋亡和炎症的多种机制。大量证据表明，由母体饮食或胎盘功能不全引起的不良宫内环境可能使胎儿对以后发生心血管、肾脏、代谢和内分泌疾病的易感性“编程”。在宫内和产后生长期间，大鼠缺锌也可被视为成年期心血管和肾脏疾病胎儿编程的模型。胎儿期、哺乳期和/或断奶后饮食限制锌会导致动脉血压升高，并损害成年期的肾功能。这篇综述重点介绍了实验和临床研究对锌在心血管和肾脏系统中的生理作用的现有知识的贡献。此外，本综述还研究了生命不同时期锌缺乏与成年期心血管和肾脏疾病发展之间的关系。
