抄録
Zinc has an essential role in growth and developmental processes. Therefore, zinc deficiency in infants can result in various disorders including growth restriction, skin lesions, and alopecia. Zinc concentrations in breast milk are considerably higher than those of the maternal serum to meet infant's requirements. Thus, effective mechanisms ensuring secretion of large amounts of zinc into the milk operate in mammary epithelial cells during lactation. Recently, the zinc transporter ZnT2 was found to play an essential role in the secretion of zinc into breast milk. Several missense mutations of ZnT2 have been identified in the mothers, who secreted low zinc breast milk, causing their breast-fed infant to develop transient neonatal zinc deficiency. This paper reviews current knowledge of transient neonatal zinc deficiency and low milk zinc concentrations caused by ZnT2 mutations, discussing the molecular basis of ZnT2 functions.
