Access to the conferences will be possible by invitation in order to obtain a connection right.
Please ask for your invitation to :
Lucretia Antonia Mota (EGIR Secretary) :
Bile acids (BA) exert important functions in the entero-hepatic system. BA are synthesized and conjugated in the liver, secreted in the duodenum after meal ingestion, modified by the intestinal gut flora, reabsorbed in the intestine and transported back to the liver by the portal vein. Although most BA are recaptured by hepatocytes, a fraction escapes and reaches peripheral organs.
BA pool size and composition are modulated by metabolic perturbations, being altered in obesity, insulin-resistance, type 2 diabetes and non-alcoholic steatohepatitis (NASH) in preclinical models and humans. BA sequestrants, which interrupt the entero-hepatic BA circulation, improve lipid/glucose homeostasis. Modification of the intestinal microbiota also alters the BA pool in mice. Systemic BA concentrations increase after Roux-en-Y-gastric-bypass (RYGB) surgery in humans and animal models.
BA modulate metabolism in part through activation of the nuclear receptor Farnesoid X Receptor (FXR) and the membrane receptor TGR5. BA and FXR regulate metabolism via entero-hepatic signalling. FXR protects the liver from BA overflow by regulating BA synthesis, secretion and transport. In the intestine, BA bind to FXR in ileal enterocytes to induce FGF15/19 expression which in turn inhibits hepatic BA synthesis. In the liver, FXR also regulates glucose and lipid metabolism. Moreover, FXR signalling contributes to the changes in gut microbial communities and the metabolic benefits of vertical sleeve gastrectomy. Furthermore, microbiota-modified BA not only act in the gut, but also on the entero-hepatic system to control hepatic BA metabolism and obesity. Intestinal FXR signalling also modulates liver function through modulation entero-endocrine L cell incretin GLP-1 and epithelial cell FGF19 production. These studies established the importance of BA receptor-mediated signalling in intestine and liver as potential targets for the treatment of metabolic diseases.
Bart Staels, PhD., Full Professor, University of Lille, France, is director of the Inserm Unit UMR 1011 with laboratories on the campus of the Institut Pasteur de Lille and the Medical Faculty of the University of Lille, Lille, France.
Pr. Staels earned his doctorate at the Institute for Pharmaceutical Sciences, University of Leuven, Belgium. He completed postdoctoral work at the Metabolic Research Unit, University of California, San Francisco and was postdoctoral research fellow of the BioAvenir Project, Paris, France. He was Senior Member of the Institut Universitaire de France (2011-16). He is co-founder and board member of the European Genomic Institute for Diabetes (EGID, Lille). He is appointed European corresponding member of the National Academy of Pharmacy (2011-) and received the International Francqui Professor Chair (2013). Pr. Staels is also co-founder of the Nasdaq-listed biopharmaceutical company Genfit SA, and president of its Scientific Advisory Board.
Pr Staels has been awarded the Young Investigator Award of the European Atherosclerosis Society, the Bronze Medal of the CNRS, the Lifetime Achievement Award of the British Atherosclerosis Society, the pharmaceutical “Barré” 207 prize from the Faculté de Pharmacie of Montreal (2007), the French “JP Binet” prize from the Fondation pour la Recherche Médicale (2011), the “Distinguished Leader in Insulin Resistance” award from the International Committee for Insulin Resistance (ICIR; 2012) and the Laurens van Deenen lecture award at the International Conference on the Bioscience of Lipids (ICBL; 2017).
Pr. Staels’ transdisciplinary research covers the fields of obesity, diabetes, hepatic and cardiovascular diseases focussing on molecular pharmacology of these cardio-metabolic diseases. He particularly studies the role of nuclear receptors (such as the PPARs, FXR, Rev-erbα and RORα) in the control of inflammation and lipid and glucose homeostasis as well as the transcriptional mechanisms involved. Pr. Staels was among the first to identify a crucial role for the nuclear receptor PPARα in the control of lipid and glucose metabolism as well as cardiovascular function in humans. He elucidated the action mechanism of the fibrate class of drugs used in the treatment of lipid disorders and worked also on the action mechanism of the glitazones, a class of anti-diabetic drugs. His work has identified the PPAR transcription factors as potential drug targets for the treatment of diabetes, dyslipidemia, cardiovascular disease and NAFLD, which contributed to the development of several novel therapeutic compounds, two of which (elafibranor and pemafibrate) are currently in phase III of clinical development. He has been invited speaker at most international congresses of the learned societies covering these disciplines, including the European Atherosclerosis Society, the International Atherosclerosis Society, the American Heart Association, the European Association for the Study of Diabetes, the American Diabetes Association, the International Diabetes Foundation, the European Association for the Study of the Liver and the American Associations for the Study of Liver Diseases meetings. He is past-president of the Nouvelle Société Française d’Athérosclérose (NSFA; 2009-2011).
Pr. Staels is also reviewer for numerous international journals. He contributed to the organization of congresses such as the “International Symposia on PPARs”, the NSFA annual congress and was chairman of Keystone Symposia on “Metabolic Syndrome” and “Genetic and Molecular Basis of Obesity and Body Weight Regulation”.
To date, Pr. Staels has published >900 papers, including 220 review articles, published abstracts and several book chapters. He received the ISI citations award, ranked in the top 35 highest publishing French researchers in the French 2007 Necker Institute dossier (2000-2005), in the 2018 Highly Cited Researchers list of Clarivate Analytics and in the Google Scholar h-index 2019 list (#314 ) (citation number of 62 107; h-index factor of 127 and average citation of 66/article).