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Altered Autophagy in Human Adipose Tissues in Obesity

Kovsan, Julia, Blüher, Matthias, Tarnovscki, Tanya, Klöting, Nora, Kirshtein, Boris, Madar, Liron, Shai, Iris, Golan, Rachel, Harman-Boehm, Ilana, Schön, Michael R., Greenberg, Andrew S., Elazar, Zvulun, Bashan, Nava, Rudich, Assaf·2011·The Journal of Clinical Endocrinology & Metabolism

Abstract

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 inc…

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Research works printed but not linked: 19

  1. Kovsan, 2010, Potential role of autophagy in modulation of lipid metabolism., Am J Physiol Endocrinol Metab, 298, E1, 10.1152/ajpendo.00562.2009 · DOI
  2. Arstila, 1968, Studies on cellular autophagocytosis. The formation of autophagic vacuoles in the liver after glucagon administration., Am J Pathol, 53, 687
  3. Shibata, 2009, The MAP1-LC3 conjugation system is involved in lipid droplet formation., Biochem Biophys Res Commun, 382, 419, 10.1016/j.bbrc.2009.03.039 · DOI · Paper page
  4. Weidberg, 2009, Lipophagy: selective catabolism designed for lipids., Dev Cell, 16, 628, 10.1016/j.devcel.2009.05.001 · DOI
  5. Singh, 2009, Autophagy regulates adipose mass and differentiation in mice., J Clin Invest, 119, 3329
  6. Zhang, 2009, Adipose-specific deletion of autophagy-related gene 7 (atg7) in mice reveals a role in adipogenesis., Proc Natl Acad Sci USA, 106, 19860, 10.1073/pnas.0906048106 · DOI · Paper page
  7. Bashan, 2007, Mitogen-activated protein kinases, inhibitory-κB kinase, and insulin signaling in human omental versus subcutaneous adipose tissue in obesity., Endocrinology, 148, 2955, 10.1210/en.2006-1369 · DOI
  8. Blüher, 2009, Activated Ask1-MKK4–p38MAPK/JNK stress signaling pathway in human omental fat tissue may link macrophage infiltration to whole-body Insulin sensitivity., J Clin Endocrinol Metab, 94, 2507, 10.1210/jc.2009-0002 · DOI
  9. Harman-Boehm, 2007, Macrophage infiltration into omental versus subcutaneous fat across different populations: effect of regional adiposity and the comorbidities of obesity., J Clin Endocrinol Metab, 92, 2240, 10.1210/jc.2006-1811 · DOI · Paper page
  10. Klöting, 2007, Serum retinol-binding protein is more highly expressed in visceral than in subcutaneous adipose tissue and is a marker of intra-abdominal fat mass., Cell Metab, 6, 79, 10.1016/j.cmet.2007.06.002 · DOI
  11. Duffaut, 2009, Interplay between human adipocytes and T lymphocytes in obesity: CCL20 as an adipochemokine and T lymphocytes as lipogenic modulators., Arterioscler Thromb Vasc Biol, 29, 1608, 10.1161/ATVBAHA.109.192583 · DOI
  12. Rudich, 2007, Adipose stress-sensing kinases: linking obesity to malfunction., Trends Endocrinol Metab, 18, 291, 10.1016/j.tem.2007.08.006 · DOI
  13. Klionsky, 2008, Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes., Autophagy, 4, 151, 10.4161/auto.5338 · DOI · Paper page
  14. Alirezaei, 2009, Elevated ATG5 expression in autoimmune demyelination and multiple sclerosis., Autophagy, 5, 152, 10.4161/auto.5.2.7348 · DOI
  15. Kiyono, 2009, Autophagy is activated by TGF-β and potentiates TGF-β-mediated growth inhibition in human hepatocellular carcinoma cells., Cancer Res, 69, 8844, 10.1158/0008-5472.CAN-08-4401 · DOI
  16. Rouschop, 2010, The unfolded protein response protects human tumor cells during hypoxia through regulation of the autophagy genes MAP1LC3B and ATG5., J Clin Invest, 120, 127, 10.1172/JCI40027 · DOI · Paper page
  17. Gesta, 2006, Evidence for a role of developmental genes in the origin of obesity and body fat distribution., Proc Natl Acad Sci USA, 103, 6676, 10.1073/pnas.0601752103 · DOI
  18. Zhou, 2009, Autophagy-mediated insulin receptor down-regulation contributes to endoplasmic reticulum stress-induced insulin resistance., Mol Pharmacol, 76, 596, 10.1124/mol.109.057067 · DOI
  19. Ost, 2010, Attenuated mTOR signaling and enhanced autophagy in adipocytes from obese patients with type 2 diabetes., Mol Med (Cambridge, Mass), 16, 235, 10.2119/molmed.2010.00023 · DOI

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Metadata

Authors
Kovsan, J., Blüher, M., Tarnovscki, T., Klöting, N., Kirshtein, B., Madar, L., Shai, I., Golan, R., Harman-Boehm, I., Schön, M. R., Greenberg, A. S., Elazar, Z., Bashan, N., & Rudich, A.
Affiliations
  • Departments of Clinical Biochemistry (J.K., T.T., L.M., N.B., A.R.) Ben-Gurion University of the Negev, Beer-Sheva 84103, Israel;
  • Department of Medicine (M.B., N.K.), University of Leipzig, D-04103 Leipzeig, Germany;
  • Department of Surgery A (B.K.) Soroka Medical Center, Beer-Sheva 84101, Israel;
  • Departments of Epidemiology (I.S., R.G.) Ben-Gurion University of the Negev, Beer-Sheva 84103, Israel;
  • Diabetes Unit (I.H.-B.), Soroka Medical Center, Beer-Sheva 84101, Israel;
  • Städtisches Klinikum Karlsruhe (M.R.S.), Clinic of Visceral Surgery, D-76133 Karlsruhe, Germany;
  • Jean Mayer Human Nutrition Research Center-U.S. Department of Agriculture Human Nutrition Research Center on Aging (A.S.G.), Tufts Univeristy, Boston, Massachusetts 02111;
  • Department of Biological Chemistry (Z.E.), The Weizmann Institute of Science, Rehovot 76100, Israel
Venue
The Journal of Clinical Endocrinology & Metabolism
Published
2011-02-01
Volume
96
Issue
2
Pages
E268-E277
ISSN
  • 0021-972X
  • 1945-7197
Cited by
301
References
6
Language
en

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