| pubmed-article:8397125 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8397125 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:8397125 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:8397125 | lifeskim:mentions | umls-concept:C0001473 | lld:lifeskim |
| pubmed-article:8397125 | lifeskim:mentions | umls-concept:C1256369 | lld:lifeskim |
| pubmed-article:8397125 | lifeskim:mentions | umls-concept:C1159756 | lld:lifeskim |
| pubmed-article:8397125 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:8397125 | pubmed:dateCreated | 1993-10-21 | lld:pubmed |
| pubmed-article:8397125 | pubmed:abstractText | Glucose-induced insulin secretion is desensitized during long-term exposure of pancreatic islet beta-cells to elevated glucose levels. This study characterizes an in vitro model of glucose-induced desensitization in cultured isolated islets of the rat. Insulin secretion in desensitized islets cultured with 11 mM glucose for 4-7 days was progressively reduced compared with the normal freshly isolated (fresh) islets. When desensitized islets were returned to a basal concentration of glucose (5.5 mM) for up to 2 h, the glucose sensitivity of insulin secretion was restored to normal (recovered islets). Carbachol and L-arginine also reversed the effects of desensitization. However, basal insulin release was elevated in desensitized and recovered islets. Sodium-dependent myo-inositol uptake was reduced during desensitization by up to 49% within 4 days. myo-Inositol uptake was restored to normal in a time-dependent manner during recovery of islets at 5.5 mM glucose. The recovery of myo-inositol uptake paralleled that of insulin release. The apparent transport constant for myo-inositol uptake was significantly increased during desensitization, whereas the maximum uptake was not changed. myo-Inositol supplementation (35 or 250 microM) during islet culture did not alter myo-inositol uptake or insulin secretion in desensitized islets. Na(+)-K(+)-ATPase activity, but not 5'-nucleotidase activity, in desensitized islets was also inhibited by 65 and 47% when compared with fresh islet and recovered islet Na(+)-K(+)-ATPase activity, respectively. Thus, cultured islets represent an appropriate model to study biochemical parameters associated with the onset and reversibility of glucose desensitization of insulin secretion.(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
| pubmed-article:8397125 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8397125 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8397125 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8397125 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:8397125 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8397125 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8397125 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8397125 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8397125 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8397125 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8397125 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8397125 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8397125 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8397125 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:8397125 | pubmed:issn | 0012-1797 | lld:pubmed |
| pubmed-article:8397125 | pubmed:author | pubmed-author:LaychockS GSG | lld:pubmed |
| pubmed-article:8397125 | pubmed:author | pubmed-author:XiaMM | lld:pubmed |
| pubmed-article:8397125 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8397125 | pubmed:volume | 42 | lld:pubmed |
| pubmed-article:8397125 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8397125 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8397125 | pubmed:pagination | 1392-400 | lld:pubmed |
| pubmed-article:8397125 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:8397125 | pubmed:meshHeading | pubmed-meshheading:8397125-... | lld:pubmed |
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| pubmed-article:8397125 | pubmed:meshHeading | pubmed-meshheading:8397125-... | lld:pubmed |
| pubmed-article:8397125 | pubmed:meshHeading | pubmed-meshheading:8397125-... | lld:pubmed |
| pubmed-article:8397125 | pubmed:meshHeading | pubmed-meshheading:8397125-... | lld:pubmed |
| pubmed-article:8397125 | pubmed:meshHeading | pubmed-meshheading:8397125-... | lld:pubmed |
| pubmed-article:8397125 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:8397125 | pubmed:articleTitle | Insulin secretion, myo-inositol transport, and Na(+)-K(+)-ATPase in glucose-desensitized rat islets. | lld:pubmed |
| pubmed-article:8397125 | pubmed:affiliation | Department of Pharmacology and Therapeutics, State University of New York at Buffalo, School of Medicine. | lld:pubmed |
| pubmed-article:8397125 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8397125 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8397125 | lld:pubmed |
