Indirect Regulation of PTH by Estrogens May Require FGF23

被引：78

作者：

Carrillo-Lopez, Natalia ^{[1
]}

Roman-Garcia, Pablo ^{[1
]}

Rodriguez-Rebollar, Ana ^{[1
]}

Luis Fernandez-Martin, Jose ^{[1
]}

Naves-Diaz, Manuel ^{[1
]}

Cannata-Andia, Jorge B. ^{[1
]}

机构：

[1] Univ Oviedo, Hosp Univ Cent Asturias, Inst Reina Sofia Invest, Bone & Mineral Res Unit,REDinREN ISCIII, E-33006 Oviedo, Asturias, Spain

来源：

JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY | 2009年 / 20卷 / 09期

关键词：

PARATHYROID-HORMONE SECRETION; VITAMIN-D METABOLISM; RETINOID-X-RECEPTOR; POSTMENOPAUSAL WOMEN; 1,25-DIHYDROXYVITAMIN-D RECEPTORS; SECONDARY HYPERPARATHYROIDISM; BIOCHEMICAL MARKERS; MINERAL METABOLISM; BONE LOSS; IN-VITRO;

D O I：

10.1681/ASN.2008121258

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

1002 ; 100201 ;

摘要：

The mechanisms by which estrogens modulate PTH are controversial, including whether or not estrogen receptors (ERs) are present in the parathyroid glands. To explore these mechanisms, we combined a rat model of CKD with ovariectomy and exogenous administration of estrogens. We found that estrogen treatment significantly decreased PTH mRNA and serum levels. We did not observe ER alpha or ER beta mRNA or protein in the parathyroids, suggesting an indirect action of estrogens on PTH regulation. Estrogen treatment significantly decreased serum 1,25(OH)(2) vitamin D-3 and phosphorus levels. In addition, estrogens significantly increased fibroblast growth factor 23 (FGF23) mRNA and serum levels. In vitro, estrogens led to transcriptional and translational upregulation of FGF23 in osteoblast-like cells in a time- and concentration-dependent manner. These results suggest that estrogens regulate PTH indirectly, possibly through FGF23.

引用

页码：2009 / 2017

页数：9

共 51 条

[31] EXPERIMENTAL UREMIA - DESCRIPTION OF A MODEL PRODUCING VARYING DEGREES OF STABLE UREMIA [J].