Talk:Nutrition: Difference between revisions
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PMID: 21291560 | PMID: 21291560 | ||
http://www.ncbi.nlm.nih.gov/pubmed/21291560 | http://www.ncbi.nlm.nih.gov/pubmed/21291560 | ||
===Vitamin D dependent rickets type I=== | |||
Korean J Pediatr. 2011 Feb;54(2):51-4. Epub 2011 Feb 28. | |||
Kim CJ. | |||
Source | |||
Department of Pediatrics, Chonnam National University Medical School, Gwangju, Korea. | |||
Abstract | |||
Vitamin D is present in two forms, ergocalciferol (vitamin D(2)) produced by plants and cholecalciferol (vitamin D(3)) produced by animal tissues or by the action of ultraviolet light on 7-dehydrocholesterol in human skin. Both forms of vitamin D are biologically inactive pro-hormones that must undergo sequential hydroxylations in the liver and the kidney before they can bind to and activate the vitamin D receptor. The hormonally active form of vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)(2)D], plays an essential role in calcium and phosphate metabolism, bone growth, and cellular differentiation. Renal synthesis of 1,25(OH)(2)D from its endogenous precursor, 25-hydroxyvitamin D (25OHD), is the rate-limiting and is catalyzed by the 1α-hydroxylase. Vitamin D dependent rickets type I (VDDR-I), also referred to as vitamin D 1α-hydroxylase deficiency or pseudovitamin D deficiency rickets, is an autosomal recessive disorder characterized clinically by hypotonia, muscle weakness, growth failure, hypocalcemic seizures in early infancy, and radiographic findings of rickets. Characteristic laboratory features are hypocalcemia, increased serum concentrations of parathyroid hormone (PTH), and low or undetectable serum concentrations of 1,25(OH)(2)D despite normal or increased concentrations of 25OHD. Recent advances have showed in the cloning of the human 1α-hydroxylase and revealed mutations in its gene that cause VDDR-I. This review presents the biology of vitamin D, and 1α-hydroxylase mutations with clinical findings. | |||
PMID: 21503197 [PubMed] PMCID: PMC3077501 | |||
http://www.ncbi.nlm.nih.gov/pubmed/21503197/ | |||
==2006== | ==2006== | ||
Revision as of 00:19, 13 August 2011
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Cite this page: Hill, M.A. (2024, April 24) Embryology Nutrition. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Nutrition |
2011
Does prenatal micronutrient supplementation improve children's mental development? A systematic review
Leung BM, Wiens KP, Kaplan BJ. BMC Pregnancy Childbirth. 2011 Feb 3;11:12. Review.
PMID: 21291560 http://www.ncbi.nlm.nih.gov/pubmed/21291560
Vitamin D dependent rickets type I
Korean J Pediatr. 2011 Feb;54(2):51-4. Epub 2011 Feb 28.
Kim CJ. Source Department of Pediatrics, Chonnam National University Medical School, Gwangju, Korea.
Abstract
Vitamin D is present in two forms, ergocalciferol (vitamin D(2)) produced by plants and cholecalciferol (vitamin D(3)) produced by animal tissues or by the action of ultraviolet light on 7-dehydrocholesterol in human skin. Both forms of vitamin D are biologically inactive pro-hormones that must undergo sequential hydroxylations in the liver and the kidney before they can bind to and activate the vitamin D receptor. The hormonally active form of vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)(2)D], plays an essential role in calcium and phosphate metabolism, bone growth, and cellular differentiation. Renal synthesis of 1,25(OH)(2)D from its endogenous precursor, 25-hydroxyvitamin D (25OHD), is the rate-limiting and is catalyzed by the 1α-hydroxylase. Vitamin D dependent rickets type I (VDDR-I), also referred to as vitamin D 1α-hydroxylase deficiency or pseudovitamin D deficiency rickets, is an autosomal recessive disorder characterized clinically by hypotonia, muscle weakness, growth failure, hypocalcemic seizures in early infancy, and radiographic findings of rickets. Characteristic laboratory features are hypocalcemia, increased serum concentrations of parathyroid hormone (PTH), and low or undetectable serum concentrations of 1,25(OH)(2)D despite normal or increased concentrations of 25OHD. Recent advances have showed in the cloning of the human 1α-hydroxylase and revealed mutations in its gene that cause VDDR-I. This review presents the biology of vitamin D, and 1α-hydroxylase mutations with clinical findings.
PMID: 21503197 [PubMed] PMCID: PMC3077501
http://www.ncbi.nlm.nih.gov/pubmed/21503197/
2006
Nutrient Reference Values for Australia and New Zealand Including Recommended Dietary Intakes
- The Nutrient Reference Values outline the levels of intake of essential nutrients considered to be adequate to meet the known nutritional needs of practically all healthy people for prevention of deficiency states. The document can be used by health professionals to assess the likelihood of inadequate intake in individuals or groups of people.
- Report used to prepare some content on topic page.
2002
http://www.scielosp.org/scielo.php?pid=S0042-96862002000800007&script=sci_arttext
