| pubmed-article:3894356 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3894356 | lifeskim:mentions | umls-concept:C0021641 | lld:lifeskim |
| pubmed-article:3894356 | lifeskim:mentions | umls-concept:C0007262 | lld:lifeskim |
| pubmed-article:3894356 | lifeskim:mentions | umls-concept:C1442792 | lld:lifeskim |
| pubmed-article:3894356 | lifeskim:mentions | umls-concept:C1515926 | lld:lifeskim |
| pubmed-article:3894356 | pubmed:issue | 17 | lld:pubmed |
| pubmed-article:3894356 | pubmed:dateCreated | 1985-9-16 | lld:pubmed |
| pubmed-article:3894356 | pubmed:abstractText | The effects of streptozotocin-induced diabetes and the subsequent treatment of diabetic animals with insulin were studied using a dose of streptozotocin that produces highly ketotic animals 48 h after injection. Carnitine palmitoyltransferase of diabetic animals had apparent Ki values for malonyl-CoA that were approximately 10 times greater than control animals, indicating a greatly decreased affinity for malonyl-CoA in the diabetic state. Subsequent treatment of diabetic animals with insulin for 5 days produced non-ketotic animals with normal blood glucose, and the affinity of carnitine palmitoyltransferase for malonyl-CoA was increased to the control level. Treatment of other groups of ketotic diabetic animals with insulin produced substantial changes in the carnitine palmitoyltransferase apparent Ki value for malonyl-CoA within 4 h. These results suggest that insulin modulates the ketotic state, at least in part, by increasing the affinity of carnitine palmitoyltransferase for malonyl-CoA to bring about inhibition of fatty acid oxidation and ketogenesis. | lld:pubmed |
| pubmed-article:3894356 | pubmed:language | eng | lld:pubmed |
| pubmed-article:3894356 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3894356 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:3894356 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3894356 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:3894356 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:3894356 | pubmed:author | pubmed-author:CookG AGA | lld:pubmed |
| pubmed-article:3894356 | pubmed:author | pubmed-author:GambleM SMS | lld:pubmed |
| pubmed-article:3894356 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3894356 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:3894356 | pubmed:volume | 260 | lld:pubmed |
| pubmed-article:3894356 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3894356 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3894356 | pubmed:pagination | 9516-9 | lld:pubmed |
| pubmed-article:3894356 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:3894356 | pubmed:year | 1985 | lld:pubmed |
| pubmed-article:3894356 | pubmed:articleTitle | Alteration of the apparent Ki of carnitine palmitoyltransferase for malonyl-CoA by the diabetic state and reversal by insulin. | lld:pubmed |
| pubmed-article:3894356 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:3894356 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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