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|dc.identifier.citation||General and Comparative Endocrinology. Vol.181, No.1 (2013), 235-240||en_US|
|dc.description.abstract||Among the reported ~300 biological actions, the established role of prolactin (PRL) is to act as a vertebrate hypercalcemic hormone that regulates epithelial calcium transport in several organs, such as the gills, intestine, and kidney. In fish, PRL stimulates the branchial calcium transport by increasing the activity of Ca2+-ATPase. Although this calciotropic hormone also induces hypercalcemia in amphibians, reptiles and birds, little has been known regarding the underlying mechanism. In contrast, the effects of PRL on the epithelial calcium transport in mammals are well documented. In rodents, PRL has been shown to stimulate the renal tubular calcium reabsorption and intestinal calcium absorption, the latter of which is mediated by the PRL-induced upregulation of calcium transporter gene expression and activities. Recently, we demonstrated that the duodenal calcium absorption in lactating rats was markedly enhanced by the suckling-induced PRL surge, presumably to provide calcium for milk production. The cellular and molecular mechanisms of the PRL-stimulated calcium transport in mammals have been elaborated in this review. © 2012 Elsevier Inc.||en_US|
|dc.subject||Biochemistry, Genetics and Molecular Biology||en_US|
|dc.title||Regulation of epithelial calcium transport by prolactin: From fish to mammals||en_US|
|Appears in Collections:||Scopus 2011-2015|
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