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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 Zn2+ for Normal Growth and Development
المؤلفون المشاركون
Miletta, Maria Consolata
Eblé, Andrée
Bieri, Andreas
Kernland, Kristin
Mullis, Primus E.
Petkovic, Vibor
Schöni, Martin H.
Flück, Christa E.
المصدر
International Journal of Endocrinology
العدد
المجلد 2013، العدد 2013 (31 ديسمبر/كانون الأول 2013)، ص ص. 1-8، 8ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2013-09-29
دولة النشر
مصر
عدد الصفحات
8
التخصصات الرئيسية
الملخص EN
Suboptimal dietary zinc (Zn2+) intake is increasingly appreciated as an important public health issue.
Zn2+ is an essential mineral, and infants are particularly vulnerable to Zn2+ deficiency, as they require large amounts of Zn2+ for their normal growth and development.
Although term infants are born with an important hepatic Zn2+ storage, adequate Zn2+ nutrition of infants mostly depends on breast milk or formula feeding, which contains an adequate amount of Zn2+ to meet the infants’ requirements.
An exclusively breast-fed 6 months old infant suffering from Zn2+ 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 Zn2+ homeostasis and dynamics.
The role of ZnTs is to reduce intracellular Zn2+ by transporting it from the cytoplasm into various intracellular organelles and by moving Zn2+ into extracellular space.
Zips increase intracellular Zn2+ by transporting it in the opposite direction.
Thus the coordinated action of both is essential for the maintenance of Zn2+ homeostasis in the cytoplasm, and accumulating evidence suggests that this is also true for the secretory pathway of growth hormone.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Miletta, Maria Consolata& Bieri, Andreas& Kernland, Kristin& Schöni, Martin H.& Petkovic, Vibor& Flück, Christa E.…[et al.]. 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 Zn2+ for Normal Growth and Development. International Journal of Endocrinology،Vol. 2013, no. 2013, pp.1-8.
https://search.emarefa.net/detail/BIM-458160
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
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 Zn2+ for Normal Growth and Development. International Journal of Endocrinology No. 2013 (2013), pp.1-8.
https://search.emarefa.net/detail/BIM-458160
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Miletta, Maria Consolata& Bieri, Andreas& Kernland, Kristin& Schöni, Martin H.& Petkovic, Vibor& Flück, Christa E.…[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 Zn2+ for Normal Growth and Development. International Journal of Endocrinology. 2013. Vol. 2013, no. 2013, pp.1-8.
https://search.emarefa.net/detail/BIM-458160
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-458160
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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