Possible roles of zinc nutriture in the fetal origins of disease

详细信息    查看全文

• 作者：Wolfgang Maret ; Harold H. S ; stead
• 关键词：Zinc deficiency ; Fetal malformations ; Disease in later life ; Epigenetics
• 刊名：Experimental Gerontology
• 出版年：2008
• 出版时间：May 2008
• 年：2008
• 卷：43
• 期：5
• 页码：378-381
• 全文大小：96 K

文摘

Risk of diseases of metabolism such as atherosclerosis and adult onset diabetes mellitus is increased by fetal malnutrition. Deficiencies of micronutrients essential for methylation are believed to contribute to the phenomenon in part through epigenetic abnormalities. Zinc is one of the nutrients essential for the epigenome. Because the worldwide prevalence of zinc deficiency is at least 20 % , fetal zinc deficiency is common. We suggest fetal zinc deficiency contributes to the pathogenesis of metabolic diseases in adults. In support of our thesis, research in experimental models and humans established the essentiality of zinc at all stages of intrauterine and infant life. Experiments in rodents and/or non-human primates found that fetal and/or suckling zinc deficiency impairs neuropsychological functions of progeny and that the effects persist in spite of nutritional rehabilitation. In addition, maternal zinc deficiency in mice is reported to impair immunity of progeny; effects persist in spite of nutritional rehabilitation into the next generation. We suspect that zinc deficiency is a far greater human health problem than is generally recognized.