Source:http://linkedlifedata.com/resource/pubmed/id/14988246
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2004-2-27
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pubmed:abstractText |
Type 2 diabetic subjects manifest both disordered insulin action and abnormalities in their pancreatic islet cells. Whether the latter represents a primary defect or is a consequence of the former is unknown. To examine the beta-cell mass and function of islets from type 2 diabetic patients directly, we isolated islets from pancreata of type 2 diabetic cadaveric donors (n = 14) and compared them with islets from normal donors (n = 14) matched for age, BMI, and cold ischemia time. The total recovered islet mass from type 2 diabetic pancreata was significantly less than that from nondiabetic control subjects (256,260 islet equivalents [2,588 IEq/g pancreas] versus 597,569 islet equivalents [6,037 IEq/g pancreas]). Type 2 diabetic islets were also noted to be smaller on average, and histologically, islets from diabetic patients contained a higher proportion of glucagon-producing alpha-cells. In vitro study of islet function from diabetic patients revealed an abnormal glucose-stimulated insulin release response in perifusion assays. In addition, in comparison with normal islets, an equivalent number of type 2 diabetic islets failed to reverse hyperglycemia when transplanted to immunodeficient diabetic mice. These results provide direct evidence for abnormalities in the islets of type 2 diabetic patients that may contribute to the pathogenesis of the disease.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0012-1797
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pubmed:author |
pubmed-author:AdamFrankF,
pubmed-author:BarkerClyde FCF,
pubmed-author:DengShaopingS,
pubmed-author:DesaiNiraj MNM,
pubmed-author:DolibaNicolaiN,
pubmed-author:HuangXiaolunX,
pubmed-author:KoeberleinBrigitteB,
pubmed-author:LianMoh-MohMM,
pubmed-author:MarkmannJames FJF,
pubmed-author:MatschinskyFranz MFM,
pubmed-author:NajiAliA,
pubmed-author:VatamaniukMarkoM,
pubmed-author:VelidedeogluErgunE,
pubmed-author:WolfBryanB
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pubmed:issnType |
Print
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pubmed:volume |
53
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
624-32
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:14988246-Age of Onset,
pubmed-meshheading:14988246-Body Mass Index,
pubmed-meshheading:14988246-Diabetes Mellitus, Type 2,
pubmed-meshheading:14988246-Humans,
pubmed-meshheading:14988246-Islets of Langerhans,
pubmed-meshheading:14988246-Islets of Langerhans Transplantation,
pubmed-meshheading:14988246-Middle Aged,
pubmed-meshheading:14988246-Organ Size,
pubmed-meshheading:14988246-Patient Selection,
pubmed-meshheading:14988246-Reference Values,
pubmed-meshheading:14988246-Retrospective Studies
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pubmed:year |
2004
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pubmed:articleTitle |
Structural and functional abnormalities in the islets isolated from type 2 diabetic subjects.
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pubmed:affiliation |
Department of Surgery, Harrison Department of Surgical Research, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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