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Mark E Cleasby, Pauline M Jamieson, and Philip J Atherton

protein metabolism. Published effects of insulin, insulin-like growth factor 1 (IGF1), amino acids, myostatin, urocortins and vitamin D on signalling pathways and effector machinery (glucose transporters, mitochondrial function, translation and activation

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R Ørnsrud, E J Lock, C N Glover, and G Flik

Introduction The fat soluble vitamins A (VA) and D (VD) are essential nutrients in the diet of vertebrates. VA is crucial for vision, growth, reproduction and embryological development. VD is deeply involved in calcium (Ca) and phosphorus (P

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Rhonda D Prisby

occur at a rapid rate as opposed to the delayed responses in bone. Vitamin D Normal development and the maintenance of the skeleton is reliant upon vitamin D (25(OH)D 3 ), such that the active form, 1α,25(OH) 2 D 3 , is involved in calcium

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J L Nobre, P C Lisboa, A P Santos-Silva, N S Lima, A C Manhães, J F Nogueira-Neto, A Cabanelas, C C Pazos-Moura, E G Moura, and E de Oliveira

calcium supplementation relies on the fact that calcium has the ability to modulate energy metabolism through calciotropic hormone concentrations: calcitriol (1,25-dihydroxyvitamin D (1,25(OH)2D)) and parathyroid hormone (PTH; Zemel 2002 ). Vitamin D

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Idris Mohamed and James K Yeh

from Hilltop Lab Animals, Inc., (Scottdale, PA, USA). They were maintained on a 12 h light:12 h darkness cycle at 22 °C with access to tap water and standard pellet diet (containing 0.93% calcium, 0.65% phosphorus, and 3 IU/g vitamin D 3 (Robert

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Hassina Ould Hamouda, Bernadette Delplanque, Yacir Benomar, Delphine Crépin, Laure Riffault, Pascale LeRuyet, Cécile Bonhomme, and Mohammed Taouis

. 2003 , Nestel et al . 2014 ), it is still necessary to study the effects of a combination of protein, lipids, and micronutrients (such as vitamin D (VitD)). This can be achieved in animal models (such as elderly rodents) of undernutrition in elderly

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S Bas, E Aguilera-Tejero, A Bas, J C Estepa, I Lopez, J A Madueño, and M Rodriguez

proliferation. Determination of calcium receptor (CaR) mRNA and vitamin D receptor (VDR) mRNA: RNA isolation and RT-PCR Parathyroid tissue samples were placed in nuclease-free 1.5 ml microcentrifuge tubes for total RNA

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T. M. Nguyen, A. Halhali, H. Guillozo, M. Garabedian, and S. Balsan

ABSTRACT

The effect of thyroparathyroidectomy (TPTX) on the plasma concentrations of the vitamin D metabolites (25-(OH)D, 24,25-(OH)2D and 1,25-(OH)2D) has been studied in pregnant rats and their fetuses during the last quarter of gestation.

Maternal and fetal vitamin D metabolites were not significantly affected by TPTX. A significant increase in plasma 1,25-(OH)2D concentrations was observed in both TPTX and control mothers and fetuses from days 19 to 21. Fetal and maternal plasma 25-(OH)D were positively correlated in both control and TPTX groups. Such a correlation was also found for 24,25-(OH)2D in the two groups. In contrast, a positive correlation between maternal and fetal plasma concentrations of 1,25-(OH)2D was found in TPTX but not in control rats.

These data suggest that major alterations in calcium metabolism, such as that produced by maternal TPTX, are insufficient to affect the changes in maternal and fetal plasma 1,25-(OH)2D during late pregnancy significantly. They also suggest that parathyroid hormone, thyroxine, and/or calcitonin may control a possible placental transfer of 1,25-(OH)2D in the rat.

J. Endocr. (1988) 116, 381–385

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N. Wongsurawat, H. J. Armbrecht, T. V. Zenser, L. R. Forte, and B. B. Davis

ABSTRACT

Growth hormone stimulates intestinal calcium absorption. This action has been linked to vitamin D metabolism. We have investigated the effects of hypophysectomy and GH treatment on renal metabolism of 25-hydroxycholecalciferol (25-OH-D3). Renal hydroxylation of 25-OH-D3 was measured in vitro using the renal slice technique. Experiments were performed in young F344 rats fed a vitamin D-replete, low calcium diet for 4 weeks. In hypophysectomized rats, renal conversion of 25-OH-D3 to 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) was markedly reduced compared with sham-operated rats. Renal conversion of 25-OH-D3 to 24,25-(OH)2D3 was markedly increased in hypophysectomized rats compared with sham-operated rats. Treatment of hypophysectomized rats with rat GH (rGH) for 10 days resulted in a significant increase in renal conversion of 25-OH-D3 to 1,25-(OH)2D3 and a significant decrease in conversion to 24,25-(OH)2D3. Rat GH treatment caused no significant changes in serum levels of immunoreactive parathyroid hormone. Serum calcium concentrations were similar in all groups, and serum phosphorus was low in hypophysectomized rats. Treatment of hypophysectomized rats with ovine GH for 6 days caused changes which were much less pronounced than those induced by rGH. Renal conversion of 25-OH-D3 to 1,25-(OH)2D3 and 24,25-(OH)2D3 correlated well with growth rate (weight gain). These results suggest that GH, either directly or indirectly, modulates renal metabolism of 25-OH-D3.

J. Endocr. (1984) 101, 333–338

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L M Atley, N Lefroy, and J D Wark

Abstract

1,25-Dihydroxyvitamin D3 (1,25-(OH)2D3) is active in primary dispersed and clonal pituitary cells where it stimulates pituitary hormone production and agonist-induced hormone release. We have studied the effect of 1,25-(OH)2D3 on thyrotropin-releasing hormone (TRH) binding in clonal rat pituitary tumour (GH3) cells. Compared with vehicle-treated cells, 1,25-(OH)2D3 (10 nmol/l) increased specific [3H]MeTRH binding by 26% at 8 h, 38% at 16 h, 35% at 24 h and reached a maximum at 48 h (90%). In dose–response experiments, specific [3H]MeTRH binding increased with 1,25-(OH)2D3 concentration and reached a maximum at 10 nmol/l. Half-maximal binding occurred at 0·5 nmol 1,25-(OH)2D3/l. The vitamin D metabolite, 25-OH D3, increased [3H]MeTRH binding but was 1000-fold less potent than 1,25-(OH)2D3. In equilibrium binding assays, treatment with 10 nmol 1,25-(OH)2D3/l for 48 h increased the maximum binding from 67·4 ± 8·8 fmol/mg protein in vehicle-treated cells to 96·7 ± 12·4 fmol/mg protein in treated cells. There was no difference in apparent K d (1·08 ± 0·10 nmol/l for 1,25-(OH)2D3-treated and 0·97 ± 0·11 nmol/l for vehicle-treated cells). Molecular investigations revealed that 10 nmol 1,25-(OH)2D3/l for 24 h caused an 8-fold increase in TRH receptor-specific mRNA. Actinomycin D (2 μg/ml, 6 h) abrogated the 1,25-(OH)2D3-induced increase in [3H]MeTRH binding. Cortisol also increased [3H]MeTRH binding but showed no additivity or synergism with 1,25-(OH)2D3. TRH-stimulated prolactin release was not enhanced by 1,25-(OH)2D3. We conclude that the active vitamin D metabolite, 1,25-(OH)2D3, caused a time- and dose-dependent increase in [3H]MeTRH binding. The effect was vitamin D metabolite-specific and resulted from an upregulation of the TRH receptor. Further studies are needed to determine the functional significance of this novel finding.

Journal of Endocrinology (1995) 147, 397–404