Linked Life Data

19795094

Source:http://linkedlifedata.com/resource/pubmed/id/19795094

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2010-2-26
pubmed:abstractText
The type III inorganic phosphate (Pi) transporter Pit-1 was previously found to be preferentially expressed in developing long bones. Several studies also described a regulation of its expression in cultured bone cells by osteotropic factors, suggesting a role of this transporter in bone metabolism. In the present study, we investigated the effects of the transgenic overexpression of Pit-1 in Wistar male rats on calcium phosphate and bone metabolism. A threefold increase and doubling of Pi transport activity were recorded in primary cultured osteoblastic cells derived from calvaria of two transgenic (Tg) lines compared with wild-type littermates (WT), respectively. Skeletal development was not affected by the transgene, and bone mass, analyzed by DXA, was slightly decreased in Tg compared with WT. Enhanced Pi uptake in calvaria-derived osteoblasts from Pit-1 Tg was associated with a significantly decreased expression of alkaline phosphatase activity and a normal deposition and calcification of the collagenous matrix. In 4-month-old adult Tg rats, serum Pi and renal Pi transport were increased compared with WT. The decrease of serum Ca concentration was associated with increased serum parathyroid hormone levels. Variations in serum Pi in Pit-1 Tg rats were negatively correlated with serum fibroblast growth factor-23, whereas 1,25-dihydroxyvitamin D(3) was not affected by Pit-1 overexpression. In conclusion, transgenic Pit-1 overexpression in rats affected bone and calcium phosphate metabolism. It also decreased alkaline phosphatase activity in osteoblasts without influencing bone matrix mineralization as well as skeletal development.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1435-5604
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
139-48
pubmed:meshHeading
pubmed-meshheading:19795094-Alanine, pubmed-meshheading:19795094-Alkaline Phosphatase, pubmed-meshheading:19795094-Animals, pubmed-meshheading:19795094-Animals, Newborn, pubmed-meshheading:19795094-Bone Density, pubmed-meshheading:19795094-Bone and Bones, pubmed-meshheading:19795094-Calcitriol, pubmed-meshheading:19795094-Calcium, pubmed-meshheading:19795094-Cell Differentiation, pubmed-meshheading:19795094-Fibroblast Growth Factors, pubmed-meshheading:19795094-Hydroxyapatites, pubmed-meshheading:19795094-Male, pubmed-meshheading:19795094-Mice, pubmed-meshheading:19795094-Osteoblasts, pubmed-meshheading:19795094-Parathyroid Hormone, pubmed-meshheading:19795094-Phosphates, pubmed-meshheading:19795094-Rats, pubmed-meshheading:19795094-Rats, Transgenic, pubmed-meshheading:19795094-Rats, Wistar, pubmed-meshheading:19795094-Skull, pubmed-meshheading:19795094-Sodium-Phosphate Cotransporter Proteins, Type III, pubmed-meshheading:19795094-Tibia
pubmed:year
2010
pubmed:articleTitle
Effects of transgenic Pit-1 overexpression on calcium phosphate and bone metabolism.
pubmed:affiliation
Division of Endocrinology and Metabolism, Department of Internal Medicine, Fujita Health University, 1-98 Dengakugakubo, Kutsukake-cho, Toyoake, Aichi, 470-1192, Japan. aslapin@fujita-hu.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't