Regulation of epithelial calcium transport by prolactin: From fish to mammals

被引:26
作者
Wongdee, Kannikar [1 ,3 ]
Charoenphandhu, Narattaphol [1 ,2 ]
机构
[1] Mahidol Univ, Fac Sci, Ctr Calcium & Bone Res COCAB, Bangkok 10400, Thailand
[2] Mahidol Univ, Fac Sci, Dept Physiol, Bangkok 10400, Thailand
[3] Burapha Univ, Fac Allied Hlth Sci, Off Acad Management, Chon Buri, Thailand
关键词
Calcium transport; Claudin; Hypercalcemia; Lactation; Prolactin; VITAMIN-D; CACO-2; MONOLAYER; GENE-EXPRESSION; DEFICIENCIES INCREASE; SIGNAL-TRANSDUCTION; CA2+ ABSORPTION; AVIAN UTERUS; RECEPTOR; METABOLISM; DUODENUM;
D O I
10.1016/j.ygcen.2012.07.006
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Among the reported similar to 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. (C) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码:235 / 240
页数:6
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