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Xinjian Peng, Nishant Tiwari, Sarbani Roy, Liang Yuan, Genoveva Murillo, Rajeshwari R Mehta, Richard V Benya, and Rajendra G Mehta

/Skip, which could interact with vitamin D receptor (VDR) and regulate vitamin D-mediated transcription and splicing ( Zhang et al . 2003 ). It is reported that a dominant negative inhibitor of NcoA62/Skip interferes with appropriate splicing of 1,25(OH

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H. PAVLOVITCH, T. L. CLEMENS, D. LAOUARI, J. L. H. O'RIORDAN, and S. BALSAN

The metabolism of 25-hydroxycholecalciferol (25-(OH)D3), plasma concentration of 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) and the amount of calcium-binding protein (CaBP) in duodenal mucosa were determined in ovariectomized rats and were compared with data observed in normal age-matched cyclic rats. Sephadex LH-20 and high-pressure liquid chromatography were used for the study of the metabolism of 25-(OH)D3. The concentration of 1,25-(OH)2D3 in plasma and prolactin in serum were measured by radioimmunoassay. Calcium-binding protein in duodenal mucosa was determined immunologically using electroimmunodiffusion. The results showed that the lack of ovarian hormones and low prolactin levels observed in ovariectomized rats did not promote a significant change in the metabolism of 25-(OH)D3, in the levels of 1,25-(OH)2D3 in the circulation or in the amount of CaBP in duodenal mucosa. It is possible that the regulation of 25-(OH)D3 by sex hormones is restricted to the state of calcium stress such as during egg-laying in birds or pregnancy and lactation in mammals.

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S Boonen, J Aerssens, and J Dequeker

Introduction

Age is the most important empirical determinant of bone mass. Factors associated with ageing account for the slow phase of bone loss, which begins in cortical bone by the age of 40 and continues throughout life at a rate of about 0·6% per year. In trabecular bone, it may begin even earlier and continues at a rate of about 0·7% per year (Burger et al. 1994, Greenspan et al. 1994, May et al. 1994). Although this loss probably reflects the aggregate effects of several processes, bone mass and bone strength depend, in part, upon calcium balance. When the amount of calcium absorbed from the diet is insufficient, calcium must be withdrawn from bone, which contains 99% of the total body stores. In both sexes, active intestinal transport of calcium decreases with ageing, particularly after the age of 70. This decrease is partially accounted for by an age-related deficiency of

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M. C. d'Emden and J. D. Wark

ABSTRACT

The hormone 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) has been shown to selectively enhance agonist-induced TSH release in the rat thyrotroph in vitro. The interaction of 1,25-(OH)2D3 with tri-iodothyronine (T3) and cortisol was studied in primary cultures of dispersed anterior pituitary cells. TRH (1 nmol/l)-induced TSH release over 1 h was enhanced by 70% (P<0·01) following exposure to 10 nmol 1,25-(OH)2D3/l for 24 h. Pretreatment with T3 (1 pmol/l–1 μmol/l) for 24 h caused a dose-dependent inhibition of TRH-induced TSH release. Net TRH-induced TSH release was inhibited by 85% at T3 concentrations of 3 nmol/l or greater. Co-incubation with 1,25-(OH)2D3 resulted in enhanced TRH-induced TSH release at all T3 concentrations tested (P<0·001). The increment of TRH-induced TSH release resulting from 1,25-(OH)2D3 pretreatment was equivalent in the presence or absence of maximal inhibitory T3 concentrations. At 1 nmol T3/1, there was a two- to threefold relative increase in 1,25-(OH)2D3-enhanced TRH-induced TSH release. Incubation with cortisol (100 pmol/l–100 nmol/l) had no effect on basal or TRH-induced TSH release, nor did it alter 1,25-(OH)2D3-enhanced TRH-induced TSH release when added 24 h before, or at the time of addition of 1,25-(OH)2D3. Actinomycin D and α-amanitin abolished 1,25-(OH)2D3-enhanced TSH secretion.

These data demonstrate that the action of 1,25-(OH)2D3 in the thyrotroph required new RNA transcription, and was not affected by cortisol. In the presence of T3, the response of the thyrotroph to TRH induced by 1,25-(OH)2D3 was increased. We have shown that 1,25-(OH)2D3 has significant effects on the action of TRH and T3 in vitro. These findings support the proposal that 1,25-(OH)2D3 may modulate TSH secretion in vivo.

Journal of Endocrinology (1989) 121, 451–458

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R. Buffenstein, D. C. Skinner, S. Yahav, G. P. Moodley, M. Cavaleros, D. Zachen, F. P. Ross, and J. M. Pettifor

ABSTRACT

The damara mole rat, Cryptomys damarensis, is a strictly subterranean dwelling herbivorous rodent that in its natural habitat has no access to any obvious source of cholecalciferol (D3). We examined the effects of D3 supplementation, at physiological and supraphysiological doses, on calcium metabolism, plasma concentrations of calcium and alkaline phosphatase (ALP) and D3 metabolites. Animals not receiving a D3 supplement maintained normal plasma calcium concentrations. In addition, they exhibited a high apparent fractional mineral absorption efficiency (91%) and maintained a positive mineral flux. The serum concentration of 25-(OH)D3 was undetectable (< 5 nmol/l) and that of 1,25-(OH)2D3 was 41±10 pmol/l. Supplementation at a physiological dose of D3 resulted in increased plasma concentrations of D3 metabolites, food intake, apparent fractional absorption efficiency and apparent fractional retention efficiency. Despite the 1·8-fold increase in food intake, body mass remained constant suggesting that the enhanced energy intake was dissipated in catabolic processes. Plasma calcium and ALP concentrations were not significantly altered with physiological doses of D3. The group given supraphysiological doses of D3 exhibited hypercalcaemia, increased creatinine concentrations and markedly increased ALP levels. These data indicate that a pathological response to D3 intoxication occurred and that hepatic and renal excretory functions were impaired. It appears, therefore, that these animals function optimally at the low concentrations of D3 metabolites found naturally. Supplementation at both physiological and supraphysiological doses of D3 may disadvantage the damara mole rat.

Journal of Endocrinology (1991) 131, 197–202

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Ankana Ganguly, Jennifer A Tamblyn, Alexandra Shattock, Annsha Joseph, Dean P Larner, Carl Jenkinson, Janesh Gupta, Janesh R Gross, and Martin Hewison

Introduction Vitamin D binding protein (DBP) is a serum globulin associated with the systemic transport of vitamin D metabolites ( Chun 2012 ). Glomerular filtration of DBP and its primary cargo, the main circulating form of vitamin D, 25

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Ichiro Kaneko, Rimpi K Saini, Kristin P Griffin, G Kerr Whitfield, Mark R Haussler, and Peter W Jurutka

Introduction The vitamin D receptor (VDR) regulates transcription in response to its 1,25-dihydroxyvitamin D 3 (1,25D) ligand by forming a heterodimer with one of the retinoid X receptors (RXRs) and binding to vitamin D responsive elements (VDREs

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Ryoko Yamamoto, Tomoko Minamizaki, Yuji Yoshiko, Hirotaka Yoshioka, Kazuo Tanne, Jane E Aubin, and Norihiko Maeda

various kinases/phosphatases; and as a regulator of intracellular signaling. The 1α,25-dihydroxyvitamin D 3 (1,25(OH) 2 D 3 )–parathyroid hormone (PTH) axis plays a major role in phosphate homeostasis, but clinical features of, for example, vitamin D

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Kenichi Serizawa, Kenji Yogo, Yoshihito Tashiro, Satoshi Takeda, Ryohei Kawasaki, Ken Aizawa, and Koichi Endo

(i.e. FMD). In estrogen-deficient postmenopausal women, brachial artery FMD was decreased as compared with premenopausal women ( Moreau et al . 2012 ). Many reports demonstrated that vitamin D, which is widely used as a supplement for osteoporosis

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Yumiko Honjo, Shigekazu Sasaki, Yoshimasa Kobayashi, Hiroko Misawa, and Hirotoshi Nakamura

enterohepatic circulation of bile acid have profound effects on the absorption and metabolism of these lipophilic ligands from the intestine. For example, severe malabsorption of D3 and vitamin A (a precursor of RA) has been reported in patients with progressive