| Altered autophagy in human adipose tissues in obesity. | |
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MedLine Citation:
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PMID: 21047928 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Context: Autophagy is a housekeeping mechanism, involved in metabolic regulation and stress response, shown recently to regulate lipid droplets biogenesis/breakdown and adipose tissue phenotype. Objective: We hypothesized that in human obesity autophagy may be altered in adipose tissue in a fat depot and distribution-dependent manner. Setting and Patients: Paired omental (Om) and subcutaneous (Sc) adipose tissue samples were used from obese and nonobese (n = 65, cohort 1); lean, Sc-obese and intraabdominally obese (n = 196, cohort 2); severely obese persons without diabetes or obesity-associated morbidity, matched for being insulin sensitive or resistant (n = 60, cohort 3). Results: Protein and mRNA levels of the autophagy genes Atg5, LC3A, and LC3B were increased in Om compared with Sc, more pronounced among obese persons, particularly with intraabdominal fat accumulation. Both adipocytes and stromal-vascular cells contribute to the expression of autophagy genes. An increased number of autophagosomes and elevated autophagic flux assessed in fat explants incubated with lysosomal inhibitors were observed in obesity, particularly in Om. The degree of visceral adiposity and adipocyte hypertrophy accounted for approximately 50% of the variance in omental Atg5 mRNA levels by multivariate regression analysis, whereas age, sex, measures of insulin sensitivity, inflammation, and adipose tissue stress were excluded from the model. Moreover, in cohort 3, the autophagy marker genes were increased in those who were insulin resistant compared with insulin sensitive, particularly in Om. Conclusions: Autophagy is up-regulated in adipose tissue of obese persons, especially in Om, correlating with the degree of obesity, visceral fat distribution, and adipocyte hypertrophy. This may co-occur with insulin resistance but precede the occurrence of obesity-associated morbidity. |
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Authors:
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Julia Kovsan; Matthias Blüher; Tanya Tarnovscki; Nora Klöting; Boris Kirshtein; Liron Madar; Iris Shai; Rachel Golan; Ilana Harman-Boehm; Michael R Schön; Andrew S Greenberg; Zvulun Elazar; Nava Bashan; Assaf Rudich |
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Publication Detail:
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Type: Journal Article Date: 2010-11-03 |
Journal Detail:
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Title: The Journal of clinical endocrinology and metabolism Volume: 96 ISSN: 1945-7197 ISO Abbreviation: J. Clin. Endocrinol. Metab. Publication Date: 2011 Feb |
Date Detail:
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Created Date: 2011-02-07 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0375362 Medline TA: J Clin Endocrinol Metab Country: United States |
Other Details:
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Languages: eng Pagination: E268-77 Citation Subset: AIM; IM |
Affiliation:
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Department of Clinical Biochemistry, Faculty of Health Sciences, National Institute of Biotechnology Negev, Ben-Gurion University of the Negev, Beer-Sheva, 84103, Israel. rudich@bgu.ac.il. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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