| The role of autophagy in β-cell lipotoxicity and type 2 diabetes. | |
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MedLine Citation:
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PMID: 21029295 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Autophagy, a ubiquitous catabolic pathway involved in both cell survival and cell death, has been implicated in many age-associated diseases. Recent findings have shown autophagy to be crucial for proper insulin secretion and β-cell viability. Transgenic mice lacking autophagy in their β-cells showed decreased β-cell mass and suppressed glucose-stimulated insulin secretion. Several studies showed that stress can stimulate autophagy in β-cells: the number of autophagosomes is increased in different in vivo models for diabetes, such as db/db mice, mice fed high-fat diet, pdx-1 knockout mice, as well as in in vitro models of glucotoxicity and lipotoxicity. Pharmacological and molecular inhibition of autophagy increases the susceptibility to cell stress, suggesting that autophagy protects against diabetes-relevant stresses. Recent findings, however, question these conclusions. Pancreases of diabetics and β-cells exposed to fatty acids show accumulation of abnormal autophagosome morphology and suppression of lysosomal gene expression suggesting impairment in autophagic turnover. In this review we attempt to give an overview of the data generated by others and by us in view of the possible role of autophagy in diabetes, a role which depending on the conditions, could be beneficial or detrimental in coping with stress. |
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Authors:
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G Las; O S Shirihai |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Diabetes, obesity & metabolism Volume: 12 Suppl 2 ISSN: 1463-1326 ISO Abbreviation: Diabetes Obes Metab Publication Date: 2010 Oct |
Date Detail:
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Created Date: 2010-10-29 Completed Date: 2011-03-09 Revised Date: 2011-12-16 |
Medline Journal Info:
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Nlm Unique ID: 100883645 Medline TA: Diabetes Obes Metab Country: England |
Other Details:
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Languages: eng Pagination: 15-9 Citation Subset: IM |
Copyright Information:
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© 2010 Blackwell Publishing Ltd. |
Affiliation:
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Department of Medicine, Section of Molecular Medicine, Boston University School of Medicine, Boston, MA 02118, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Autophagy / physiology* Diabetes Mellitus, Experimental / metabolism, physiopathology* Diabetes Mellitus, Type 2 / metabolism, physiopathology* Fatty Acids / metabolism* Humans Insulin-Secreting Cells / metabolism* Lysosomes / genetics, physiology* Mice Mice, Transgenic |
| Grant Support | |
ID/Acronym/Agency:
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R01 DK035914-26/DK/NIDDK NIH HHS; R01 DK056690-12/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Fatty Acids |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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