Adiponectin upregulates monocytic activin A but systemic levels are not altered in obesity or type 2 diabetes |
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| Authors: | Johanna Weigert Markus Neumeier Josef Wanninger Franziska Schober Daniela Sporrer Markus Weber Andrea Schramm Sylvia Wurm Fabian Stögbauer Michael Filarsky Andreas Schäffler Charalampos Aslanidis Jürgen Schölmerich Christa Buechler |
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| Affiliation: | 1. Graduate School of Medical Science, Kumamoto Health Science University, Kumamoto, Japan;2. Graduate School of Medical Sciences, Kumamoto University Medical School, Kumamoto, Japan;1. University of Groningen, University Medical Center Groningen, Department of Cardiology, Groningen, The Netherlands;2. Eindhoven University of Technology, Department of Mathematics and Computer Science, Eindhoven, The Netherlands;3. University of Groningen, University Medical Center Groningen, Department of Nephrology, Groningen, The Netherlands;1. Institute for Functional and Applied Anatomy, Hannover Medical School, Hannover, Germany;2. Clinic for Oral and Maxillofacial Surgery, Henriettenstiftung, Hannover, Germany;3. Clinic for General- and Visceral Surgery, Section of Pediatric Surgery, University Clinic Ulm, Ulm, Germany;4. Department of Trauma Surgery, Hannover Medical School, Hannover, Germany;5. Department of Anatomy and Cell Biology, Martin Luther University, Faculty of Medicine, Halle (Saale), Germany |
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| Abstract: | Adiponectin is an adipocyte-derived protein with atheroprotective and immunoregulatory function. Adiponectin and activin A reduce foam cell formation and adiponectin activates the p38 MAPK pathway that is well described to induce activin A. Therefore, it was analyzed whether adiponectin alters activin A in primary human monocytes. Adiponectin dose- and time-dependently induced activin A in the supernatant, and the maximal amount was observed after 12 h of incubation. Adiponectin-stimulated release of activin A was blocked by a p38 MAPK inhibitor. Metformin and pioglitazone are drugs frequently used to treat diabetic patients and metformin slightly reduced monocytic activin A release whereas pioglitazone had no effect. Type 2 diabetes is associated with elevated inflammatory systemic cytokines but activin A serum levels were similar in slim probands, overweight controls and type 2 diabetic patients. Furthermore, activin A did not correlate to systemic adiponectin, body mass index, waist to hip ratio or C-reactive protein. These findings indicate that adiponectin upregulates monocytic activin A release via the p38 MAPK pathway, and this may in part explain the immunoregulatory and antiatherosclerotic effects of this adipokine. |
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