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Role of P38mapk in Palmitate-Induced Inflammation in C2C12 Muscle Cells Alexandre Pinel, Jean-Paul Rigaudière, Béatrice Morio, Frédéric Capel

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Role of P38mapk in Palmitate-Induced Inflammation in C2C12 Muscle Cells Alexandre Pinel, Jean-Paul Rigaudière, Béatrice Morio, Frédéric Capel Role of p38MAPK in palmitate-induced inflammation in C2C12 muscle cells Alexandre Pinel, Jean-Paul Rigaudière, Béatrice Morio, Frédéric Capel To cite this version: Alexandre Pinel, Jean-Paul Rigaudière, Béatrice Morio, Frédéric Capel. Role of p38MAPK in palmitate-induced inflammation in C2C12 muscle cells. 13. International Congress on Obesity, May 2016, Vancouver, Canada. Obesity Reviews, 17 (suppl. S2), pp.1-215, 2016, Obesity Reviews. 10.1111/obr.12398. hal-01595375 HAL Id: hal-01595375 https://hal.archives-ouvertes.fr/hal-01595375 Submitted on 3 Jun 2020 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. ABSTRACTS Track1: From genes to cells fl T1:S1:03 Session 1: Adipose in ammation and HemeOxygenase and Met-inflammation remodelling Esterbauer, H.* Medizinische Universität Wien T1:S1:01 No abstract submitted Immune Cell Cross-talk In Adipose Tissue Bouloumié, A.* l’Institut National de la Santé et de la Recherche Médicale T1:S1:04 Adipose tissue (AT) is constituted by adipocytes and distinct cell types, Cellular origins of fibrosis the so called stroma-vascular fraction (SVF), that define the adipocyte Clement, K.* microenvironment. SVF contains progenitor cells, vascular cells and Institute of Cardiometabolisme and Nutrition (ICAN), immune cells, mainly lymphocytes and macrophages. Flow cytometry INSERM, Sorbonne University analyses performed on SVF showed that the adipocyte microenviron- Fibrosis occurs in many organs including the white adipose tissue ment is dependent on both fat depot location (subcutaneous and vis- (WAT) as a result of prolonged tissue injury with exaggerated extra- ceral AT) and adiposity degree. Phenotypes, numbers and cell cellular matrix deposition. This phenomenon causes tissue disorga- subsets of macrophages and lymphocytes are strongly modulated in nization and functional alterations. Whereas not completely adepot-specific manner by obesity, weight loss as well as nutritional understood, fibrotic transformation in several organs is mediated conditions. To note, differences must be taken into account depending by cell activation towards a so-called myofibroblast phenotype, on species (human versus murine models). which includes matrix generation, high responsiveness to proin- The causes of AT immune cell remodeling are certainly plural. Alter- flammatory cytokines, active proliferation and sometimes resis- ations in oxygen tension and lipid metabolism, but also aging- and tance to apoptosis. In WAT depots from obese subjects, fibrosis is microflora-dependent mechanisms may be contributing events in AT now seen as part of pathological alterations associated with inflam- immune cell infiltration, resident cell proliferation and/or shift in im- mation and metabolic alterations. In the last years, our team pro- mune cell phenotypes. The consequences of such changes will impact vided description of WAT tissue remodelling and fibrosis in on AT endocrine and metabolic functions. Locally, AT immune cell various forms of obesity and during weight changes. WAT fibrosis cross-talk with progenitor cells modify their differentiation potentials is linked to changes in tissue stiffness and both fibrosis and changes including white and brite adipogenesis as well as myofibroblast poten- of stiffness appeared as contributors of metabolic deteriorations tials. In addition, interactions with mature adipocytes affect lipolysis and of unfavourable clinical outcomes after weight loss-induced and lipogenesis functions, and with endothelial cells modulate angio- bariatric surgery in severe obesity. Ex vitro and in vitro experiments genesis, leading to a global alteration of the adipose tissue buffering showed that fibrosis-embedded hypertrophied adipocytes displayed capacity to cope with excess fatty acids. Moreover, AT immune cells altered metabolic functions and increased expression/production of through the release of pro-inflammatory factors could also impact many inflammatory and fibrotic mediators partially via the stimula- on systemic metabolic and inflammatory responses. Such local and tion of mechano-sensitive pathways. New data are now being pro- systemic changes have repercussion on energy homeostasis. Therefore duced regarding cell progenitors driving human WAT fibrotic AT immune cells are major players in obesity-associated pathologies. phenotype and their phenotypic changes under various metabolic T1:S1:02 conditions and stress. New results will be presented on this matter. Adipose tissue expandability, lipotoxicity and the metabolic syndrome Vidal-Puig, A.* Session 2: Brown and beige fat University of Cambridge The link between obesity and type 2 diabetes is clear on an epidemiolog- T1:S2:02 ical level, however the mechanism linking these two common disorders BMP2, 4 and 7 exhibit distinct brite adipogenic is not well defined. One hypothesis linking obesity to type 2 diabetes is potential according to the modulation of MSCA1 the adipose tissue expandability hypothesis. The adipose tissue expand- activity ability hypothesis states that a failure in the capacity for adipose tissue Esteve, D.* Boulet, N. Belles, C. Zakaroff-Girard, A. expansion, rather than obesity per se is the key factor linking positive Decaunes, P. Bouloumié, A. and Galitzky, J. energy balance and type 2 diabetes. All individuals possess a maximum INSERM UMR1048/I2MC capacity for adipose expansion which is determined by both genetic and environmental factors. Once the adipose tissue expansion limit is Brite adipogenesis may be of potential interest to fight against obe- reached, adipose tissue ceases to store energy efficiently and lipids begin sity and to ameliorate metabolic parameters. Bone morphogenetic to accumulate in other tissues. Ectopic lipid accumulation in non- proteins (BMPs) have been described as potent brite inducers. Our adipocyte cells causes lipotoxic insults including insulin resistance, apo- previous study showed that MSCA1 is expressed by human ptosis and inflammation. This article discusses the links between bipotent committed progenitor cells and that MSCA1 activity is in- adipokines, inflammation, adipose tissue expandability and volved in brite adipogenesis. The present study aimed to character- lipotoxicity. Finally, we will discuss how considering the concept of ize the impact of BMP2, 4 or 7 on MSCA1 activity and on the allostasis may enable a better understanding of how diabetes develops modulation of mitochondrial architecture as a readout of functional and allow the rational design of new anti diabetic treatments. brite adipogenesis. © 2016 The Authors 5 obesity reviews © 2016 World Obesity 17 (Suppl. 2), 5–20, April 2016 6 Abstracts obesity reviews Human native progenitor cells (CD45-/CD34+/CD31-) and to promote energy expenditure in these end points is dependent on preadipocytes (CD45-/CD34+/CD31-/MSCA1+) were isolated from an understanding their innervation. human subcutaneous ATand cultured under adipogenic condition after Male SD rats were housed either at 27 oC or 8oC for 7 days after 48h BMP pretreatment. Adipogenesis was assessed by lipid accumula- which they were perfused with aldehydes or killed prior to removal tion and adipogenic related gene expression. The mitochondrial net- of the inguinal (iWAT) or interscapular (isBAT) brown fat and their work architecture was assessed by super-resolution microscopy associated sympathetic ganglia (iWAT = T13/L1; isBAT = stellate). BMP2, 4 or 7 pretreatment led to increased lipid accumulation and RNA was extracted from sympathetic ganglia and RNA seq was adipogenic-related gene expression.. BMP7 only increased the brite- re- used to identify differential gene expression after cold exposure. lated gene expression and MSCA1 activity. Isolated MSCA1+ At 8oC, iWAT expressed beige characteristics in the form of islands preadipocytes pretreated with BMP7 exhibited fragmented mitochon- of UCP1+ve brown-like fat which attracted elevated levels of neural drial network after adipogenic differentiation while preadipocytes input and the T13/L1 ganglion took on a brown like neurochemical pretreated with BMP2 or 4 exhibited elongated mitochondria. signature. Bioinformatics analyses revealed key candidate pathways The present study shows that among the tested BMPs, BMP7 only and neurochemicals such as CGRP within ganglionic neurons that promotes the appearance of functional brite adipocytes were specific to beige fat. No conflict of interest is disclosed. Financial support: Sanofi, These data provide the first clear insights into the nature of the spe- INSER cific neural input to beige fat. T1:S2:03 T1:S2:05 Brown and beige/brite Can both display a mammary Cold exposure induces proliferation of mature brown myoepithelial cell phenotype in vivo adipocytes: Possible role of Beta3-adrenergic 1 1 1 1 2 Li, L.* ; Li, B.G. ; Wang, G.L. ; Niu, C.Q. ; Wan, Z.J. and receptor stimulation *1 Speakman, J.R. Fukano, K.F.* Okamatsu-Ogura, Y.O. 1Institute of Genetics and Developmental Biology Chinese 2 Kobayashi-Nio, J.K. and Kimura, K.K. Academy of Sciences; Institute of Zoology Chinese Hokkaido University Academy of Sciences
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