| Autophagy: roles in obesity-induced ER stress and adiponectin downregulation in adipocytes. | |
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MedLine Citation:
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PMID: 20864818 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Accumulating evidence strongly suggests that autophagy, which is induced by endoplasmic reticulum (ER) stress in adipocytes, may play an important role in obesity-induced insulin resistance and type 2 diabetes. Obesity induces ER stress in mouse adipose tissue, which correlates with reduced adiponectin levels. In 3T3-L1 adipocytes, induction of ER stress is sufficient to promote autophagy-dependent adiponectin degradation. In contrast, suppressing ER stress increases adiponectin levels in 3T3-L1 adipocytes and alleviates high fat diet-induced adiponectin downregulation in mice. The ER stress-induced adiponectin downregulation can also be suppressed by overexpression of DsbA-L, a newly identified protein involved in promoting adiponectin multimerization and stability. Taken together, our results show that ER stress-induced autophagy provides an important mechanism underlying obesity-induced adiponectin downregulation in adipocytes. In addition, increasing the expression levels of DsbA-L could be an effective approach to improve adiponectin biosynthesis and stability, thus improving insulin sensitivity: in cells and in vivo. |
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Authors:
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Lijun Zhou; Feng Liu |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2010-11-16 |
Journal Detail:
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Title: Autophagy Volume: 6 ISSN: 1554-8635 ISO Abbreviation: Autophagy Publication Date: 2010 Nov |
Date Detail:
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Created Date: 2010-11-16 Completed Date: 2011-03-02 Revised Date: 2011-11-18 |
Medline Journal Info:
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Nlm Unique ID: 101265188 Medline TA: Autophagy Country: United States |
Other Details:
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Languages: eng Pagination: 1196-7 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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3T3-L1 Cells Adipocytes / metabolism* Adiponectin / genetics*, metabolism Animals Autophagy* Cell Survival Down-Regulation / genetics* Endoplasmic Reticulum / metabolism, pathology* Energy Metabolism Humans Mice Models, Biological Obesity / genetics*, pathology* Stress, Physiological |
| Grant Support | |
ID/Acronym/Agency:
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R01 DK76902/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Adiponectin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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