| Item type |
文献 / Documents(1) |
| 公開日 |
2020-12-25 |
| アクセス権 |
|
|
アクセス権 |
open access |
| 資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
journal article |
| 出版社版DOI |
|
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.1038/s41467-019-10189-x |
|
|
言語 |
ja |
|
|
関連名称 |
10.1038/s41467-019-10189-x |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| タイトル |
|
|
タイトル |
Diabetes causes marked inhibition of mitochondrial metabolism in pancreatic β-cells |
|
言語 |
en |
| 著者 |
Haythorne, Elizabeth
Rohm, Maria
van de Bunt, Martijn
Brereton, Melissa F.
Tarasov, Andrei I.
Blacker, Thomas S.
Sachse, Gregor
Silva dos Santos, Mariana
Terron Exposito, Raul
Davis, Simon
馬場, 麻人
Fischer, Roman
Duchen, Michael R.
Rorsman, Patrik
MacRae, James I.
Ashcroft, Frances M.
|
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
Diabetes is a global health problem caused primarily by the inability of pancreatic β-cells to secrete adequate levels of insulin. The molecular mechanisms underlying the progressive failure of β-cells to respond to glucose in type-2 diabetes remain unresolved. Using a combination of transcriptomics and proteomics, we find significant dysregulation of major metabolic pathways in islets of diabetic βV59M mice, a non-obese, eulipidaemic diabetes model. Multiple genes/proteins involved in glycolysis/gluconeogenesis are upregulated, whereas those involved in oxidative phosphorylation are downregulated. In isolated islets, glucose-induced increases in NADH and ATP are impaired and both oxidative and glycolytic glucose metabolism are reduced. INS-1 β-cells cultured chronically at high glucose show similar changes in protein expression and reduced glucose-stimulated oxygen consumption: targeted metabolomics reveals impaired metabolism. These data indicate hyperglycaemia induces metabolic changes in β-cells that markedly reduce mitochondrial metabolism and ATP synthesis. We propose this underlies the progressive failure of β-cells in diabetes. |
|
言語 |
en |
| 書誌情報 |
en : Nature Communications
巻 10,
p. 2474,
発行日 2019-06-06
|
| 収録物ID |
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収録物識別子タイプ |
ISSN |
|
収録物識別子 |
20411723 |
| 収録物ID |
|
|
収録物識別子タイプ |
NCID |
|
収録物識別子 |
AA12645905 |
| 出版者 |
|
|
出版者 |
Springer Nature |
|
言語 |
en |
| 権利情報 |
|
|
言語 |
en |
|
権利情報 |
This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
| EID |
|
|
識別子 |
353544 |
|
識別子タイプ |
URI |
| 言語 |
|
|
言語 |
eng |
ncomms_10_2474.pdf (2.28 MB)
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