| pubmed-article:12120915 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12120915 | lifeskim:mentions | umls-concept:C0521324 | lld:lifeskim |
| pubmed-article:12120915 | lifeskim:mentions | umls-concept:C0151686 | lld:lifeskim |
| pubmed-article:12120915 | lifeskim:mentions | umls-concept:C0086272 | lld:lifeskim |
| pubmed-article:12120915 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:12120915 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:12120915 | pubmed:dateCreated | 2002-7-17 | lld:pubmed |
| pubmed-article:12120915 | pubmed:abstractText | Uncontrolled diabetes is associated with growth retardation. We investigated the effect of insulin-dependent diabetes on animal growth and IGF-I gene expression in the epiphyseal growth plate region of the long bones. We also studied the effect of GH administration on somatic growth in the diabetic state. Streptozotocin (STZ)-injected diabetic rats had a decreased somatic growth rate in comparison to controls. GH administration (2.5 U/kg day) in the diabetic animals (DGH group) prevented this decrease. Serum IGF-I levels were decreased in both diabetic and DGH animals. Within 72 h from diabetes onset, IGF-I mRNA levels in epiphyseal growth plate homogenates decreased whereas IGF-I receptor mRNA levels increased in diabetic animals. The decrease in IGF-I mRNA transcript levels was localized to the metaphyseal region by in situ hybridization. We conclude that in the STZ-induced diabetic state, the reduction in linear growth is associated with a parallel decrease in IGF-I gene expression at the epiphyseal growth plate area. Diabetic growth retardation can be reversed with GH administration, which does not reconstitute serum IGF-I levels. Therefore, we speculate that GH in this model may act locally through the skeletal GH-IGF-I system. | lld:pubmed |
| pubmed-article:12120915 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12120915 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12120915 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12120915 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12120915 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12120915 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12120915 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12120915 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12120915 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12120915 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:12120915 | pubmed:issn | 0940-5429 | lld:pubmed |
| pubmed-article:12120915 | pubmed:author | pubmed-author:LandauDD | lld:pubmed |
| pubmed-article:12120915 | pubmed:author | pubmed-author:WeinrebMM | lld:pubmed |
| pubmed-article:12120915 | pubmed:author | pubmed-author:SegevYY | lld:pubmed |
| pubmed-article:12120915 | pubmed:author | pubmed-author:PhillipMM | lld:pubmed |
| pubmed-article:12120915 | pubmed:author | pubmed-author:Davidoff-Frie... | lld:pubmed |
| pubmed-article:12120915 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12120915 | pubmed:volume | 39 | lld:pubmed |
| pubmed-article:12120915 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12120915 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12120915 | pubmed:pagination | 61-7 | lld:pubmed |
| pubmed-article:12120915 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:12120915 | pubmed:meshHeading | pubmed-meshheading:12120915... | lld:pubmed |
| pubmed-article:12120915 | pubmed:meshHeading | pubmed-meshheading:12120915... | lld:pubmed |
| pubmed-article:12120915 | pubmed:meshHeading | pubmed-meshheading:12120915... | lld:pubmed |
| pubmed-article:12120915 | pubmed:meshHeading | pubmed-meshheading:12120915... | lld:pubmed |
| pubmed-article:12120915 | pubmed:meshHeading | pubmed-meshheading:12120915... | lld:pubmed |
| pubmed-article:12120915 | pubmed:meshHeading | pubmed-meshheading:12120915... | lld:pubmed |
| pubmed-article:12120915 | pubmed:meshHeading | pubmed-meshheading:12120915... | lld:pubmed |
| pubmed-article:12120915 | pubmed:meshHeading | pubmed-meshheading:12120915... | lld:pubmed |
| pubmed-article:12120915 | pubmed:meshHeading | pubmed-meshheading:12120915... | lld:pubmed |
| pubmed-article:12120915 | pubmed:meshHeading | pubmed-meshheading:12120915... | lld:pubmed |
| pubmed-article:12120915 | pubmed:meshHeading | pubmed-meshheading:12120915... | lld:pubmed |
| pubmed-article:12120915 | pubmed:meshHeading | pubmed-meshheading:12120915... | lld:pubmed |
| pubmed-article:12120915 | pubmed:meshHeading | pubmed-meshheading:12120915... | lld:pubmed |
| pubmed-article:12120915 | pubmed:meshHeading | pubmed-meshheading:12120915... | lld:pubmed |
| pubmed-article:12120915 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12120915 | pubmed:articleTitle | Involvement of the skeletal GH-IGF system in an experimental model of diabetes-induced growth retardation. | lld:pubmed |
| pubmed-article:12120915 | pubmed:affiliation | Department of Microbiology and Immunology, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer Sheva, Israel. | lld:pubmed |
| pubmed-article:12120915 | pubmed:publicationType | Journal Article | lld:pubmed |
