Publication: Regulation of epithelial calcium transport by prolactin: From fish to mammals
1
Issued Date
2013-01-05
Resource Type
ISSN
10956840
00166480
00166480
Other identifier(s)
2-s2.0-84873058836
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
General and Comparative Endocrinology. Vol.181, No.1 (2013), 235-240
Suggested Citation
Kannikar Wongdee, Narattaphol Charoenphandhu Regulation of epithelial calcium transport by prolactin: From fish to mammals. General and Comparative Endocrinology. Vol.181, No.1 (2013), 235-240. doi:10.1016/j.ygcen.2012.07.006 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/31378
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Regulation of epithelial calcium transport by prolactin: From fish to mammals
Author(s)
Other Contributor(s)
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.
