Metformin modulates lipolysis and inflammation through the modulation of T cell priming in obese-induced Type II diabetic mice

Event Abstract Back to Event Metformin modulates lipolysis and inflammation through the modulation of T cell priming in obese-induced Type II diabetic mice Seulmee Shin1, Bobae Hyun1, Aeri Lee1, Sungwon Lee1, Hyunseok Kong1, Shinha Han1, Youngcheon Song1 and Kyungjae Kim1* 1 Sahmyook University, Republic of Korea Inflammation is regarded as a key process underlying metabolic diseases in obese individuals where adipose tissue shows features characteristic of active local inflammation. Metformin is used for treating of T2D and have been suggested that metformin has anti-inflammatory properties. This study investigated the therapeutic effect of metformin on diabetic symptoms in DIO mice. Here we show metformin attenuates metabolic disorder in DIO mice and suppresses MHC-restricted antigen presentation in DCs. Metformin decreased aipogenesis related genes, FAS, SCD-1, GPAT, SREBP1a, and lipases, LPL, ATGL, HSL, but also suppressed innate cytokines expression through APPL1-AMPK-sirt1 signaling. Metformin decreased both class I- and class II-restricted presentation of exogenous OVA in DCs. Metformin also decreased expression of the co-stimulatory molecules, ICAM-1 and B7-1/-2, and MHC class I and II molecules but not phagocytic activity. Metformin decreased MHC class II-restricted exogenous antigen presentation in peritoneal macrophages in vivo. These results show that metformin attenuates adipogenesis and suppresses immune responses through APPL1-AMPK-sirt1-NF-κB signaling and followed by decreases MHC-restricted presentation of exogenous antigen. Theses finding suggests that modulation of the antigen presentation pathway by metformin could provide a novel means for regulating T cell responses in terms of controlling of inflammation in metabolic diseases. Keywords: Metformin, Lipolysis, Inflammation, Dendritic Cells, Antigen Presentation Conference: 15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013. Presentation Type: Abstract Topic: Immune-mediated disease pathogenesis Citation: Shin S, Hyun B, Lee A, Lee S, Kong H, Han S, Song Y and Kim K (2013). Metformin modulates lipolysis and inflammation through the modulation of T cell priming in obese-induced Type II diabetic mice. Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI). doi: 10.3389/conf.fimmu.2013.02.00185 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: 11 Mar 2013; Published Online: 22 Aug 2013. * Correspondence: Prof. Kyungjae Kim, Sahmyook University, Seoul, Republic of Korea, kinkj@syu.ac.kr 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 Seulmee Shin Bobae Hyun Aeri Lee Sungwon Lee Hyunseok Kong Shinha Han Youngcheon Song Kyungjae Kim Google Seulmee Shin Bobae Hyun Aeri Lee Sungwon Lee Hyunseok Kong Shinha Han Youngcheon Song Kyungjae Kim Google Scholar Seulmee Shin Bobae Hyun Aeri Lee Sungwon Lee Hyunseok Kong Shinha Han Youngcheon Song Kyungjae Kim PubMed Seulmee Shin Bobae Hyun Aeri Lee Sungwon Lee Hyunseok Kong Shinha Han Youngcheon Song Kyungjae Kim 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.