| Serum metabolite profiles and target tissue gene expression define the effect of cholecalciferol intake on calcium metabolism in rats and mice. | |
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MedLine Citation:
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PMID: 18492843 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We studied the effect of cholecalciferol (VD3) intake on VD3 status and markers of calcium (Ca) homeostasis in mice and rats. Serum 25 hydroxycholecalciferol (25OH-VD3) concentrations were increased in animals fed diets containing 400-20,000 international units (IU) VD3/kg (37 nmol.L(-1).1000 IU VD3(-1)), but body weight, serum Ca, and duodenal gene expression were not altered. High-VD3 intake decreased serum 1, 25-dihydroxycholecalciferol [1,25(OH)2-VD3] and renal 25 hydroxycholecalciferol-1alphahydroxylase (CYP27B1) mRNA, suggesting that rodents tolerate high-VD3 intake by suppressing the activity of the VD3 endocrine system. Serum 25OH-VD3 declined when animals were fed diets containing 1000 to 25 IU VD3/kg (9-11 wk, inflection at 200 IU/kg, 4-fold steeper slope below this). Neither body weight nor serum Ca were influenced by low-VD3 intake. However, mice fed the 25-IU/kg diet had lower serum 1,25(OH)2-VD3, duodenal calbindin D9k mRNA, bone mineral density, and renal 25 hydroxycholecalciferol-24 hydroxylase mRNA, whereas renal CYP27B1 mRNA was elevated when rodents were fed < 200 IU VD3/kg. These data reveal a stress on VD3 and Ca metabolism at low dietary VD3 intake. Dietary Ca restriction (0.25 vs. 0.5%, 9 wk) increased serum 1,25(OH)2-VD3 and was 30% greater in rats fed a 10,000-IU VD3/kg diet. High-VD3 intake did not prevent Ca restriction-induced bone loss. Our data show that modeling human VD3 status requires lower intake than the current NRC rodent requirement (1000-IU/kg diet). Also, although rodents are very tolerant of high-VD3 intake, it cannot compensate for moderate Ca restriction. |
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Authors:
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James C Fleet; Christy Gliniak; Zhentao Zhang; Yingben Xue; Kathleen B Smith; Rebecca McCreedy; Sunday A Adedokun |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: The Journal of nutrition Volume: 138 ISSN: 1541-6100 ISO Abbreviation: J. Nutr. Publication Date: 2008 Jun |
Date Detail:
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Created Date: 2008-05-21 Completed Date: 2008-06-23 Revised Date: 2011-09-26 |
Medline Journal Info:
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Nlm Unique ID: 0404243 Medline TA: J Nutr Country: United States |
Other Details:
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Languages: eng Pagination: 1114-20 Citation Subset: IM |
Affiliation:
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Department of Foods and Nutrition and the Interdepartmental Nutrition Program, Purdue University, West Lafayette, IN 47907-2059, USA. fleet@purdue.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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25-Hydroxyvitamin D3 1-alpha-Hydroxylase
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metabolism Animals Calcium / metabolism* Calcium, Dietary / pharmacology* Cholecalciferol / administration & dosage, blood*, metabolism* Diet Female Femur / chemistry, physiology Gene Expression Regulation / drug effects* Hydroxycholecalciferols / blood Male Mice Mice, Inbred C57BL RNA, Messenger / genetics, metabolism Random Allocation Rats Rats, Sprague-Dawley Steroid Hydroxylases / genetics, metabolism |
| Grant Support | |
ID/Acronym/Agency:
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CA101113/CA/NCI NIH HHS; DK054111/DK/NIDDK NIH HHS; R01 CA101113-04/CA/NCI NIH HHS; R01 DK054111-10/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Calcium, Dietary; 0/Hydroxycholecalciferols; 0/RNA, Messenger; 67-97-0/Cholecalciferol; 7440-70-2/Calcium; EC 1.14.-/25-Hydroxyvitamin D3 1-alpha-Hydroxylase; EC 1.14.-/Steroid Hydroxylases; EC 1.14.13.-/vitamin D 24-hydroxylase |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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