| http://purl.uniprot.org/citations/12021187 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12021187 | http://www.w3.org/2000/01/rdf-schema#comment | "Nutritional status is a critical factor that modulates the responsiveness of the liver to GH and the resulting production of endocrine (mostly liver-derived) IGF-I. Using a conditional Cre/lox P system, we have established a liver-specific IGF-I-deficient mouse model. Despite the reduction in the circulating IGF-I (75%), the growth parameters are normal, except for the reduced spleen size, providing a unique model to study the effect of protein restriction on the autocrine/paracrine GH/IGF-I axis. To determine the effects of protein calorie malnutrition on the spleen, liver-specific IGF-I-deficient mice were assigned to one of four isocaloric diets, differing in the protein content (20, 12, 4, and 0%), for a period of 10 d. A low protein intake decreased the nonhepatic IGF-I secretion into the circulation, whereas it caused an increase in the level of circulating GH. This supports the view that nonhepatic IGF-I production contributes to circulating IGF-I levels. The lack of dietary protein led to an up-regulation of GH and IGF-I receptors expression in the spleen, whereas the IGF-I mRNA remained unchanged, as was demonstrated by flow cytometry and ribonuclease protection assay. B lymphocytes seem to be responsible for the up-regulated GH/IGF-I receptor expression. Northern blot analysis showed an up-regulation of IGF-binding protein-3 mRNA levels, which suggests that the protein deprivation may lead to an increased sequestration of circulating or locally synthesized IGF-I. These results support the hypothesis that the splenic GH/IGF-I axis responds to the nutritional stress caused by a low protein intake, to maintain the tissue homeostasis."xsd:string |
| http://purl.uniprot.org/citations/12021187 | http://purl.org/dc/terms/identifier | "doi:10.1210/endo.143.6.8852"xsd:string |
| http://purl.uniprot.org/citations/12021187 | http://purl.uniprot.org/core/author | "Yakar S."xsd:string |
| http://purl.uniprot.org/citations/12021187 | http://purl.uniprot.org/core/author | "Sanchez-Gomez M."xsd:string |
| http://purl.uniprot.org/citations/12021187 | http://purl.uniprot.org/core/author | "LERoith D."xsd:string |
| http://purl.uniprot.org/citations/12021187 | http://purl.uniprot.org/core/author | "Naranjo W.M."xsd:string |
| http://purl.uniprot.org/citations/12021187 | http://purl.uniprot.org/core/author | "Perez A.U."xsd:string |
| http://purl.uniprot.org/citations/12021187 | http://purl.uniprot.org/core/author | "Setser J."xsd:string |
| http://purl.uniprot.org/citations/12021187 | http://purl.uniprot.org/core/date | "2002"xsd:gYear |
| http://purl.uniprot.org/citations/12021187 | http://purl.uniprot.org/core/name | "Endocrinology"xsd:string |
| http://purl.uniprot.org/citations/12021187 | http://purl.uniprot.org/core/pages | "2233-2241"xsd:string |
| http://purl.uniprot.org/citations/12021187 | http://purl.uniprot.org/core/title | "Protein calorie restriction affects nonhepatic IGF-I production and the lymphoid system: studies using the liver-specific IGF-I gene-deleted mouse model."xsd:string |
| http://purl.uniprot.org/citations/12021187 | http://purl.uniprot.org/core/volume | "143"xsd:string |
| http://purl.uniprot.org/citations/12021187 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/12021187 |
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