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Bile Acid Receptors as Signal Integrators in Liver and Metabolism
In the last decade, bile acids have enjoyed a real renaissance, sparked by the
identification at the turn of the millennium of their dedicated receptors, FXR
and TGR5. This has been instrumental in revealing the key role bile acids play
in regulating liver and metabolic homeostasis, transforming them from detergents
facilitating the intestinal absorption of nutrients into versatile hormones.
Signaling through FXR and TGR5 indeed modulates several metabolic pathways,
regulating not only bile acid synthesis and enterohepatic recirculation, but
also lipid, glucose and energy homeostasis. In addition, FXR and TGR5 agonists
display anti-inflammatory and anti-fibrotic properties, making these agents
interesting candidates for the treatment of several liver and metabolic
diseases, including nonalcoholic steatohepatitis (NASH). With the hepatitis C
virus infection nearly solved, NASH is already a medical problem of epidemic
proportions poised to become by 2020 the leading indication for liver
transplantation in the US. This conference will review genetics, structure and
functions of bile acid receptors and will explore the intricate interactions
among gut microbiota, bile acids and liver disease, as well as the multiple
bidirectional signals along the gut-liver axis. Intriguingly, FXR agonists, like
the bile acid derivative obeticholic acid, could have a beneficial role in the
treatment of NASH by decreasing hepatic lipogenesis, steatosis and insulin
resistance, while also inhibiting inflammatory and fibrogenic responses able to
promote liver cirrhosis and hepatocellular carcinoma. The conference therefore
aims at integrating basic, translational and clinical aspects of bile acid
receptors, bringing together an interdisciplinary group of scientists to discuss
the state of the art and propose new avenues of investigation in this active and
No meeting documents found.
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© 2018 DiaComp.org
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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