Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1976-3-15
pubmed:abstractText
Vitamin D3 gives rise to at least one hormone in which the kidney is utilized as an endocrine system. This hormone arises from 25-OH-D3 which in turn is synthesized in the liver from vitamin D3. The production of this calcium and phosphorus mobilizing hormone, namely 1,25-(OH)2D3, is strongly regulated by the need for calcium and phosphorus. The regulation of its production can occur only after initial 1,25-(OH)2D3 is made and brings about the appearance of 25-OH-D3-24hydroxylase. The need for calcium brings about a stimulation of parathyroid hormone secretion. The parathyroid hormone suppresses the 24-hydroxylase and stimulates the 1-hydroxylase. Alternatively, the need for phosphorus directly stimulates the 1-hydroxylase and suppresses the 24-hydroxylase. The 24-hydroxylation appears to be the initial reaction leading to the inactivation and excretion of vitamin D whereas the 1-hydroxylation is the reaction bringing about the activation of the molecule to 1,25-(OH)2D3. The 1,25-(OH)2D3, the 25-OH-D3 and an analog of 1,25-(OH)2D3, namely 1alpha-OH-D3, are potentially extremely useful in the treatment of metabolic bone diseases such as renal osteodystrophy, hepatically related disorders of calcium and bone metabolism, hypoparathyroidism, and vitamin D dependency disease. The 1alpha-OH-D3 is effective by virtue of its conversion to 1,25-(OH)2D3. The 25-hydroxylation of both 1alpha-OH-D3 and vitamin D3 itself occurs predominantly in the liver. Finally, it is not entirely settled whether 1,25-(OH)2D3 is active directly in all of the functions of viramin D or whether it must be further converted metabolically. A new metabolic pathway for vitamin D has been discovered in which 1,25-(OH)2D3 loses its 26 and 27 carbons to carbon dioxide, producing an unknown metabolite. It is not certain whether this pathway represents degradation of the 1,25-(OH)2D3 or its further activation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-2143
pubmed:author
pubmed:issnType
Print
pubmed:volume
87
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7-26
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:173767-25-Hydroxyvitamin D3 1-alpha-Hydroxylase, pubmed-meshheading:173767-Animals, pubmed-meshheading:173767-Bone Development, pubmed-meshheading:173767-Calcium, pubmed-meshheading:173767-Cholecalciferol, pubmed-meshheading:173767-Dihydroxycholecalciferols, pubmed-meshheading:173767-Humans, pubmed-meshheading:173767-Hydroxycholecalciferols, pubmed-meshheading:173767-Intestinal Mucosa, pubmed-meshheading:173767-Kidney, pubmed-meshheading:173767-Liver, pubmed-meshheading:173767-Muscles, pubmed-meshheading:173767-Parathyroid Glands, pubmed-meshheading:173767-Phosphorus, pubmed-meshheading:173767-Renal Osteodystrophy, pubmed-meshheading:173767-Steroid Hydroxylases, pubmed-meshheading:173767-Structure-Activity Relationship, pubmed-meshheading:173767-Vitamin D, pubmed-meshheading:173767-Vitamin D Deficiency
pubmed:year
1976
pubmed:articleTitle
Recent advances in our understanding of the vitamin D endocrine system.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review