| pubmed-article:8612577 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8612577 | lifeskim:mentions | umls-concept:C0021289 | lld:lifeskim |
| pubmed-article:8612577 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
| pubmed-article:8612577 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:8612577 | lifeskim:mentions | umls-concept:C1274040 | lld:lifeskim |
| pubmed-article:8612577 | lifeskim:mentions | umls-concept:C1334133 | lld:lifeskim |
| pubmed-article:8612577 | lifeskim:mentions | umls-concept:C0599894 | lld:lifeskim |
| pubmed-article:8612577 | lifeskim:mentions | umls-concept:C1521840 | lld:lifeskim |
| pubmed-article:8612577 | lifeskim:mentions | umls-concept:C0332453 | lld:lifeskim |
| pubmed-article:8612577 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:8612577 | pubmed:dateCreated | 1996-6-6 | lld:pubmed |
| pubmed-article:8612577 | pubmed:abstractText | Targeted disruption of the insulin receptor gene (Insr) in the mouse was achieved using the homologous recombination approach. Insr+/- mice were normal as shown by glucose tolerance tests. Normal Insr-/- pups were born at expected rates, indicating that Insr can be dispensable for intrauterine development, growth and metabolism. However, they rapidly developed diabetic ketoacidosis accompanied by a marked post-natal growth retardation (up to 30-40% of littermate size), skeletal muscle hypotrophy and fatty infiltration of the liver and they died within 7 days after birth. Total absence of the insulin receptor (IR), demonstrated in the homozygous mutant mice, also resulted in other metabolic disorders: plasma triglyceride level could increase 6-fold and hepatic glycogen content could be five times less as compared with normal littermates. The very pronounced hyperglycemia in Insr-/- mice could result in an increased plasma insulin level of up to approximately 300 microU/ml, as compared with approximately 25 microU/ml for normal littermates. However, this plasma level was still unexpectedly low when compared with human infants with leprechaunism, who lack IR but who could have extremely high insulinemia (up to > 4000 microU/ml). The pathogenesis resulting from a null mutation in Insr is discussed. | lld:pubmed |
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| pubmed-article:8612577 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8612577 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8612577 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8612577 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8612577 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:8612577 | pubmed:issn | 0261-4189 | lld:pubmed |
| pubmed-article:8612577 | pubmed:author | pubmed-author:JamiJJ | lld:pubmed |
| pubmed-article:8612577 | pubmed:author | pubmed-author:BucchiniDD | lld:pubmed |
| pubmed-article:8612577 | pubmed:author | pubmed-author:MonthiouxEE | lld:pubmed |
| pubmed-article:8612577 | pubmed:author | pubmed-author:JoshiR LRL | lld:pubmed |
| pubmed-article:8612577 | pubmed:author | pubmed-author:LamotheBB | lld:pubmed |
| pubmed-article:8612577 | pubmed:author | pubmed-author:MesbahKK | lld:pubmed |
| pubmed-article:8612577 | pubmed:author | pubmed-author:CordonnierNN | lld:pubmed |
| pubmed-article:8612577 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8612577 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:8612577 | pubmed:volume | 15 | lld:pubmed |
| pubmed-article:8612577 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8612577 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8612577 | pubmed:pagination | 1542-7 | lld:pubmed |
| pubmed-article:8612577 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:8612577 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8612577 | pubmed:articleTitle | Targeted disruption of the insulin receptor gene in the mouse results in neonatal lethality. | lld:pubmed |
| pubmed-article:8612577 | pubmed:affiliation | Institut Cochin de Génétique Moléculaire, INSERM U257, Paris, France. | lld:pubmed |
| pubmed-article:8612577 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8612577 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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