| pubmed-article:21641386 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21641386 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:21641386 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:21641386 | lifeskim:mentions | umls-concept:C0011860 | lld:lifeskim |
| pubmed-article:21641386 | lifeskim:mentions | umls-concept:C0439849 | lld:lifeskim |
| pubmed-article:21641386 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:21641386 | lifeskim:mentions | umls-concept:C0011560 | lld:lifeskim |
| pubmed-article:21641386 | lifeskim:mentions | umls-concept:C0445223 | lld:lifeskim |
| pubmed-article:21641386 | lifeskim:mentions | umls-concept:C1552599 | lld:lifeskim |
| pubmed-article:21641386 | lifeskim:mentions | umls-concept:C1704787 | lld:lifeskim |
| pubmed-article:21641386 | lifeskim:mentions | umls-concept:C1517945 | lld:lifeskim |
| pubmed-article:21641386 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:21641386 | pubmed:dateCreated | 2011-6-6 | lld:pubmed |
| pubmed-article:21641386 | pubmed:abstractText | Amyloid deposition and reduced ?-cell mass are pathological hallmarks of the pancreatic islet in type 2 diabetes; however, whether the extent of amyloid deposition is associated with decreased ?-cell mass is debated. We investigated the possible relationship and, for the first time, determined whether increased islet amyloid and/or decreased ?-cell area quantified on histological sections is correlated with increased ?-cell apoptosis. Formalin-fixed, paraffin-embedded human pancreas sections from subjects with (n = 29) and without (n = 39) diabetes were obtained at autopsy (64 ± 2 and 70 ± 4 islets/subject, respectively). Amyloid and ? cells were visualized by thioflavin S and insulin immunolabeling. Apoptotic ? cells were detected by colabeling for insulin and by TUNEL. Diabetes was associated with increased amyloid deposition, decreased ?-cell area, and increased ?-cell apoptosis, as expected. There was a strong inverse correlation between ?-cell area and amyloid deposition (r = -0.42, P < 0.001). ?-Cell area was selectively reduced in individual amyloid-containing islets from diabetic subjects, compared with control subjects, but amyloid-free islets had ?-cell area equivalent to islets from control subjects. Increased amyloid deposition was associated with ?-cell apoptosis (r = 0.56, P < 0.01). Thus, islet amyloid is associated with decreased ?-cell area and increased ?-cell apoptosis, suggesting that islet amyloid deposition contributes to the decreased ?-cell mass that characterizes type 2 diabetes. | lld:pubmed |
| pubmed-article:21641386 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21641386 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21641386 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21641386 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21641386 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21641386 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21641386 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21641386 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21641386 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21641386 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21641386 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:21641386 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21641386 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21641386 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:21641386 | pubmed:issn | 1525-2191 | lld:pubmed |
| pubmed-article:21641386 | pubmed:author | pubmed-author:WestermarkGun... | lld:pubmed |
| pubmed-article:21641386 | pubmed:author | pubmed-author:WestermarkPer... | lld:pubmed |
| pubmed-article:21641386 | pubmed:author | pubmed-author:KahnSteven... | lld:pubmed |
| pubmed-article:21641386 | pubmed:author | pubmed-author:HullRebecca... | lld:pubmed |
| pubmed-article:21641386 | pubmed:author | pubmed-author:FlignerCorinn... | lld:pubmed |
| pubmed-article:21641386 | pubmed:author | pubmed-author:ZraikaSakeneh... | lld:pubmed |
| pubmed-article:21641386 | pubmed:author | pubmed-author:CarrDarcy BDB | lld:pubmed |
| pubmed-article:21641386 | pubmed:author | pubmed-author:Aston-Mourney... | lld:pubmed |
| pubmed-article:21641386 | pubmed:author | pubmed-author:UdayasankarJa... | lld:pubmed |
| pubmed-article:21641386 | pubmed:author | pubmed-author:SubramanianSh... | lld:pubmed |
| pubmed-article:21641386 | pubmed:author | pubmed-author:JurgensCather... | lld:pubmed |
| pubmed-article:21641386 | pubmed:author | pubmed-author:ToukatlyMirna... | lld:pubmed |
| pubmed-article:21641386 | pubmed:copyrightInfo | Copyright © 2011 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved. | lld:pubmed |
| pubmed-article:21641386 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21641386 | pubmed:volume | 178 | lld:pubmed |
| pubmed-article:21641386 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21641386 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21641386 | pubmed:pagination | 2632-40 | lld:pubmed |
| pubmed-article:21641386 | pubmed:meshHeading | pubmed-meshheading:21641386... | lld:pubmed |
| pubmed-article:21641386 | pubmed:meshHeading | pubmed-meshheading:21641386... | lld:pubmed |
| pubmed-article:21641386 | pubmed:meshHeading | pubmed-meshheading:21641386... | lld:pubmed |
| pubmed-article:21641386 | pubmed:meshHeading | pubmed-meshheading:21641386... | lld:pubmed |
| pubmed-article:21641386 | pubmed:meshHeading | pubmed-meshheading:21641386... | lld:pubmed |
| pubmed-article:21641386 | pubmed:meshHeading | pubmed-meshheading:21641386... | lld:pubmed |
| pubmed-article:21641386 | pubmed:meshHeading | pubmed-meshheading:21641386... | lld:pubmed |
| pubmed-article:21641386 | pubmed:meshHeading | pubmed-meshheading:21641386... | lld:pubmed |
| pubmed-article:21641386 | pubmed:meshHeading | pubmed-meshheading:21641386... | lld:pubmed |
| pubmed-article:21641386 | pubmed:meshHeading | pubmed-meshheading:21641386... | lld:pubmed |
| pubmed-article:21641386 | pubmed:meshHeading | pubmed-meshheading:21641386... | lld:pubmed |
| pubmed-article:21641386 | pubmed:meshHeading | pubmed-meshheading:21641386... | lld:pubmed |
| pubmed-article:21641386 | pubmed:meshHeading | pubmed-meshheading:21641386... | lld:pubmed |
| pubmed-article:21641386 | pubmed:meshHeading | pubmed-meshheading:21641386... | lld:pubmed |
| pubmed-article:21641386 | pubmed:year | 2011 | lld:pubmed |
| pubmed-article:21641386 | pubmed:articleTitle | ?-cell loss and ?-cell apoptosis in human type 2 diabetes are related to islet amyloid deposition. | lld:pubmed |
| pubmed-article:21641386 | pubmed:affiliation | Division of Metabolism, Endocrinology and Nutrition, Veterans Affairs Puget Sound Health Care System and University of Washington, Seattle, Washington, USA. | lld:pubmed |
| pubmed-article:21641386 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:21641386 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:21641386 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:21641386 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
