COST BM0602 - Adipose Tissue: A Key Target for Prevention of the Metabolic Syndrome

Abstract

Event Abstract Back to Event COST BM0602 - Adipose Tissue: A Key Target for Prevention of the Metabolic Syndrome Juergen Eckel1* 1 German Diabetes Center, Germany COST BM0602 - Adipose Tissue: A Key Target for Prevention of the Metabolic Syndrome 1. Analysis of the central regulation of food intake and adipocyte storage function. The main objective of this part of the Action is to identify new molecular targets that may serve to control food intake and to prevent the development of the metabolic syndrome. An additional specific objective is to promote our knowledge on glucose sensing systems and their role in the control of energy homeostasis and body weight. Adipose cell size is critically related to glucose tolerance and insulin sensitivity. Therefore, a major goal is to understand how hypertrophy of adipose cells leads to impaired lipid storage capacity, impaired adipogenesis and systemic insulin resistance. 2. Elucidation of adipose tissue secretory function. The main objective of this research task is to comprehensively explore the regulation of adipose tissue secretory function, the origin of secretory products within the tissue, the actions of these products at the local and peripheral levels and the pathophysiological relevance for humans. Additional objectives include the identification of novel secretory products and the investigation of the pathophysiological role of the adipose tissue and its secretory products in human or animal models of the metabolic syndrome and type 2 diabetes. 3. Assessment of the relationship between cytokines, inflammation and vascular dysfunction and skeletal muscle insulin resistance.One main objective is to identify the downstream targets of the crosstalk between adipose tissue-derived proinflammatory cytokines and vascular endothelial and smooth muscle cells. This will be essential to develop new therapeutic strategies for prevention of the secondary complications associated with the metabolic syndrome and type 2 diabetes. Attempts will also be made to uncover potential synergistic interactions between cytokines, hyperglycemia and increased levels of free fatty acids. 4. Gluco-lipotoxicity, islet inflammation, beta cell dysfunction and type 2 diabetes. The main objective is to expand the current research on glucose- and free fatty acid-induced damage to beta cells to the role of adipose tissue-derived factors (i.e., proinflammatory cytokines) on the function of beta cells in such adverse environment. Detailed understanding of the molecular mechanisms that lead to beta cell apoptosis and dysfunction is essential for developing new strategies to prevent or delay the onset of type 2 diabetes. Conference: Pharmacology and Toxicology of the Blood-Brain Barrier: State of the Art, Needs for Future Research and Expected Benefits for the EU, Brussels, Belgium, 11 Feb - 12 Feb, 2010. Presentation Type: Oral Presentation Topic: Presentations Citation: Eckel J (2010). COST BM0602 - Adipose Tissue: A Key Target for Prevention of the Metabolic Syndrome. Front. Pharmacol. Conference Abstract: Pharmacology and Toxicology of the Blood-Brain Barrier: State of the Art, Needs for Future Research and Expected Benefits for the EU. doi: 10.3389/conf.fphar.2010.02.00020 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 10 Mar 2010; Published Online: 10 Mar 2010. * Correspondence: Juergen Eckel, German Diabetes Center, Duesseldorf, Germany, eckel@uni-duesseldorf.de Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Juergen Eckel Google Juergen Eckel Google Scholar Juergen Eckel PubMed Juergen Eckel Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.