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rdf:type |
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lifeskim:mentions |
umls-concept:C0086860,
umls-concept:C0205214,
umls-concept:C0205419,
umls-concept:C0681850,
umls-concept:C1256369,
umls-concept:C1421314,
umls-concept:C1550501,
umls-concept:C1706203,
umls-concept:C1880177,
umls-concept:C1882417,
umls-concept:C2349001,
umls-concept:C2697811
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pubmed:issue |
5
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pubmed:dateCreated |
2003-4-28
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pubmed:abstractText |
It was reported that the common -866G/A polymorphism in the promoter of the human uncoupling protein-2 (UCP2) gene, which enhances its trascriptional activity, is associated with increased mRNA levels in human adipocytes and reduced risk of obesity. Studies in knockout mice and beta-cells indicate that UCP2 may play a role in beta-cell function. In this study, we addressed the question of whether the common -866G/A polymorphism in UCP2 gene contributes to the variation of insulin secretion in humans by genotyping 301 nondiabetic subjects who underwent an oral glucose tolerance test. Glucose-stimulated insulin secretion estimated by several indexes of beta-cell function was significantly lower in carriers of the -866A/A genotype compared with -866A/G or -866G/G according to the dosage of the A allele (P = 0.002-0.05). To investigate directly whether the UCP2 -866G/A polymorphism affects human islet function, pancreatic islets isolated from two -866G/G homozygous, seven -866G/A heterozygous, and one -866A/A homozygous nondiabetic donors were studied. Islets from -866A/A homozygous had lower insulin secretion in response to glucose stimulation as compared with -866G/G and -866G/A carriers. These results indicate that the common -866G/A polymorphism in the UCP2 gene may contribute to the biological variation of insulin secretion in humans.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0012-1797
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pubmed:author |
pubmed-author:CardelliniMarinaM,
pubmed-author:D'AdamoMonicaM,
pubmed-author:De NicolaisPierluigiP,
pubmed-author:Del GuerraSilviaS,
pubmed-author:Del PratoStefanoS,
pubmed-author:FedericiMassimoM,
pubmed-author:FrontoniSimonaS,
pubmed-author:GambardellaSergioS,
pubmed-author:LauroDavideD,
pubmed-author:LauroRenatoR,
pubmed-author:MarchettiPieroP,
pubmed-author:MariniMaria AdelaideMA,
pubmed-author:SbracciaPaoloP,
pubmed-author:SestiGiorgioG
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pubmed:issnType |
Print
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pubmed:volume |
52
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1280-3
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:12716765-Adult,
pubmed-meshheading:12716765-Blood Glucose,
pubmed-meshheading:12716765-Female,
pubmed-meshheading:12716765-Gene Expression Regulation,
pubmed-meshheading:12716765-Genotype,
pubmed-meshheading:12716765-Glucose Tolerance Test,
pubmed-meshheading:12716765-Hemoglobin A, Glycosylated,
pubmed-meshheading:12716765-Humans,
pubmed-meshheading:12716765-Insulin,
pubmed-meshheading:12716765-Ion Channels,
pubmed-meshheading:12716765-Lipids,
pubmed-meshheading:12716765-Male,
pubmed-meshheading:12716765-Membrane Transport Proteins,
pubmed-meshheading:12716765-Middle Aged,
pubmed-meshheading:12716765-Mitochondrial Proteins,
pubmed-meshheading:12716765-Polymorphism, Single Nucleotide,
pubmed-meshheading:12716765-Promoter Regions, Genetic,
pubmed-meshheading:12716765-Proteins,
pubmed-meshheading:12716765-Transcription, Genetic
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pubmed:year |
2003
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pubmed:articleTitle |
A common polymorphism in the promoter of UCP2 contributes to the variation in insulin secretion in glucose-tolerant subjects.
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pubmed:affiliation |
Dipartimento di Medicina Sperimentale e Clinica, Università di Catanzaro-Magna Graecia, Via Tommaso Campanella, 115 11800 Catanzaro, Italy. sesti@unicz.it
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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