| pubmed-article:12669271 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12669271 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:12669271 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:12669271 | lifeskim:mentions | umls-concept:C0022131 | lld:lifeskim |
| pubmed-article:12669271 | lifeskim:mentions | umls-concept:C0061355 | lld:lifeskim |
| pubmed-article:12669271 | lifeskim:mentions | umls-concept:C1533698 | lld:lifeskim |
| pubmed-article:12669271 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:12669271 | lifeskim:mentions | umls-concept:C0439810 | lld:lifeskim |
| pubmed-article:12669271 | lifeskim:mentions | umls-concept:C1518896 | lld:lifeskim |
| pubmed-article:12669271 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:12669271 | pubmed:dateCreated | 2003-4-1 | lld:pubmed |
| pubmed-article:12669271 | pubmed:abstractText | Long-term total parenteral nutrition (TPN) is associated with elevated plasma lipids and a marked decrease of glucose-stimulated insulin release. Since nitric oxide (NO) has been shown to modulate negatively the insulin response to glucose, we investigated the influence of TPN-treatment on isoforms of islet NO-synthase (NOS) activities in relation to the effect of glucagon-like peptide-1 (GLP-1), a known activator of glucose-stimulated insulin release. Isolated islets from TPN rats incubated at basal glucose (1 mmol/l) showed a modestly increased insulin secretion accompanied by an enhanced accumulation of islet cAMP and cGMP. In contrast, TPN islets incubated at high glucose (16.7 mmol/l) displayed an impaired insulin secretion and a strong suppression of islet cAMP content. Moreover, islet inducible NOS (iNOS) as well as islet cGMP content were greatly increased in these TPN islets. A dose-response study of GLP-1 with glucose-stimulated islets showed that GLP-1 could overcome and completely restore the impaired insulin release in TPN islets, bringing about a marked increase in islet cAMP accumulation concomitant with heavy suppression of both glucose-stimulated increase in islet cGMP content and the activities of constitutive NOS (cNOS) and iNOS. These effects of GLP-1 were mimicked by dibutyryl-cAMP. The present results show that the impaired insulin response of glucose-stimulated insulin release seen after TPN treatment is normalized by GLP-1. This beneficial effect of GLP-1 is most probably exerted by a cAMP-induced suppression of both iNOS and cNOS activities in these TPN islets. | lld:pubmed |
| pubmed-article:12669271 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12669271 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12669271 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12669271 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12669271 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:12669271 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12669271 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12669271 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12669271 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12669271 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12669271 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12669271 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12669271 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:12669271 | pubmed:issn | 0018-5043 | lld:pubmed |
| pubmed-article:12669271 | pubmed:author | pubmed-author:EkelundMM | lld:pubmed |
| pubmed-article:12669271 | pubmed:author | pubmed-author:LundquistII | lld:pubmed |
| pubmed-article:12669271 | pubmed:author | pubmed-author:SalehiAA | lld:pubmed |
| pubmed-article:12669271 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12669271 | pubmed:volume | 35 | lld:pubmed |
| pubmed-article:12669271 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12669271 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12669271 | pubmed:pagination | 48-54 | lld:pubmed |
| pubmed-article:12669271 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:12669271 | pubmed:meshHeading | pubmed-meshheading:12669271... | lld:pubmed |
| pubmed-article:12669271 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12669271 | pubmed:articleTitle | Total parenteral nutrition-stimulated activity of inducible nitric oxide synthase in rat pancreatic islets is suppressed by glucagon-like peptide-1. | lld:pubmed |
| pubmed-article:12669271 | pubmed:affiliation | Department of Physiological Sciences, Division of Pharmacology, University of Lund, Sweden. salehi@farm.lu.se | lld:pubmed |
| pubmed-article:12669271 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12669271 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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