Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
10
|
| pubmed:dateCreated |
1993-10-21
|
| 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)
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Arginine,
http://linkedlifedata.com/resource/pubmed/chemical/Carbachol,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Potassium-Exchanging ATPase,
http://linkedlifedata.com/resource/pubmed/chemical/Tritium
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Oct
|
| pubmed:issn |
0012-1797
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
42
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1392-400
|
| pubmed:dateRevised |
2011-11-17
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| pubmed:meshHeading |
pubmed-meshheading:8397125-Animals,
pubmed-meshheading:8397125-Arginine,
pubmed-meshheading:8397125-Biological Transport,
pubmed-meshheading:8397125-Carbachol,
pubmed-meshheading:8397125-Cells, Cultured,
pubmed-meshheading:8397125-Disease Models, Animal,
pubmed-meshheading:8397125-Dose-Response Relationship, Drug,
pubmed-meshheading:8397125-Glucose,
pubmed-meshheading:8397125-Hyperglycemia,
pubmed-meshheading:8397125-Inositol,
pubmed-meshheading:8397125-Insulin,
pubmed-meshheading:8397125-Islets of Langerhans,
pubmed-meshheading:8397125-Male,
pubmed-meshheading:8397125-Rats,
pubmed-meshheading:8397125-Rats, Sprague-Dawley,
pubmed-meshheading:8397125-Sodium,
pubmed-meshheading:8397125-Sodium-Potassium-Exchanging ATPase,
pubmed-meshheading:8397125-Time Factors,
pubmed-meshheading:8397125-Tritium
|
| pubmed:year |
1993
|
| pubmed:articleTitle |
Insulin secretion, myo-inositol transport, and Na(+)-K(+)-ATPase in glucose-desensitized rat islets.
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| pubmed:affiliation |
Department of Pharmacology and Therapeutics, State University of New York at Buffalo, School of Medicine.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
|