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Miletta MC, Bieri A, Kernland K, et al. Transient Neonatal Zinc Deficiency Caused by a Heterozygous G87R Mutation in the Zinc Transporter ZnT-2 (SLC30A2) Gene in the Mother Highlighting the Importance of Zn (2+) for Normal Growth and Development. Int J Endocrinol. 2013;2013:259189doi: 10.1155/2013/259189.
Miletta, M. C., Bieri, A., Kernland, K., Schöni, M. H., Petkovic, V., Flück, C. E., Eblé, A., & Mullis, P. E. (2013). Transient Neonatal Zinc Deficiency Caused by a Heterozygous G87R Mutation in the Zinc Transporter ZnT-2 (SLC30A2) Gene in the Mother Highlighting the Importance of Zn (2+) for Normal Growth and Development. International journal of endocrinology, 2013259189. https://doi.org/10.1155/2013/259189
Miletta, Maria Consolata, et al. "Transient Neonatal Zinc Deficiency Caused by a Heterozygous G87R Mutation in the Zinc Transporter ZnT-2 (SLC30A2) Gene in the Mother Highlighting the Importance of Zn (2+) for Normal Growth and Development." International journal of endocrinology vol. 2013 (2013): 259189. doi: https://doi.org/10.1155/2013/259189
Miletta MC, Bieri A, Kernland K, Schöni MH, Petkovic V, Flück CE, Eblé A, Mullis PE. Transient Neonatal Zinc Deficiency Caused by a Heterozygous G87R Mutation in the Zinc Transporter ZnT-2 (SLC30A2) Gene in the Mother Highlighting the Importance of Zn (2+) for Normal Growth and Development. Int J Endocrinol. 2013;2013:259189. doi: 10.1155/2013/259189. Epub 2013 Sep 29. PMID: 24194756; PMCID: PMC3804372.
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Int J Endocrinol. 2013;2013:259189. doi: 10.1155/2013/259189. Epub 2013 Sep 29.

Transient Neonatal Zinc Deficiency Caused by a Heterozygous G87R Mutation in the Zinc Transporter ZnT-2 (SLC30A2) Gene in the Mother Highlighting the Importance of Zn (2+) for Normal Growth and Development.

International journal of endocrinology

Maria Consolata Miletta, Andreas Bieri, Kristin Kernland, Martin H Schöni, Vibor Petkovic, Christa E Flück, Andrée Eblé, Primus E Mullis

Affiliations

  1. Division of Paediatric Endocrinology, Diabetology and Metabolism and Department of Clinical Research, University Children's Hospital, Inselspital, 3010 Bern, Switzerland.

PMID: 24194756 PMCID: PMC3804372 DOI: 10.1155/2013/259189

Abstract

Suboptimal dietary zinc (Zn(2+)) intake is increasingly appreciated as an important public health issue. Zn(2+) is an essential mineral, and infants are particularly vulnerable to Zn(2+) deficiency, as they require large amounts of Zn(2+) for their normal growth and development. Although term infants are born with an important hepatic Zn(2+) storage, adequate Zn(2+) nutrition of infants mostly depends on breast milk or formula feeding, which contains an adequate amount of Zn(2+) to meet the infants' requirements. An exclusively breast-fed 6 months old infant suffering from Zn(2+) deficiency caused by an autosomal dominant negative G87R mutation in the Slc30a2 gene (encoding for the zinc transporter 2 (ZnT-2)) in the mother is reported. More than 20 zinc transporters characterized up to date, classified into two families (Slc30a/ZnT and Slc39a/Zip), reflect the complexity and importance of maintaining cellular Zn(2+) homeostasis and dynamics. The role of ZnTs is to reduce intracellular Zn(2+) by transporting it from the cytoplasm into various intracellular organelles and by moving Zn(2+) into extracellular space. Zips increase intracellular Zn(2+) by transporting it in the opposite direction. Thus the coordinated action of both is essential for the maintenance of Zn(2+) homeostasis in the cytoplasm, and accumulating evidence suggests that this is also true for the secretory pathway of growth hormone.

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