Hepatic Carbohydrate Response Element Binding Protein Activation Limits Nonalcoholic Fatty Liver Disease Development in a Mouse Model for Glycogen Storage Disease Type 1a.

Yu LeiJoanne A HoogerlandVincent W BloksTrijnie BosAycha BleekerHenk WoltersJustina Clarinda WoltersBrenda S HijmansTheo H van Dijk Rachel Thomas Michel van Weeghel Gilles Mithieux Riekelt H L Houtkooper Alain de Bruin Fabienne Rajas Folkert Kuipers Maaike H Oosterveer

Published in: Hepatology (Baltimore, Md.) (2020)

Attenuation of hepatic ChREBP induction in GSD 1a liver aggravates hepatomegaly because of further accumulation of glycogen and lipids as a result of reduced glycolysis and suppressed VLDL-TG secretion. TM6SF2, critical for VLDL formation, was identified as a ChREBP target in mouse liver. Altogether, our data show that enhanced ChREBP activity limits NAFLD development in GSD 1a by balancing hepatic TG production and secretion.

Keyphrases

mouse model
binding protein
electronic health record
big data
machine learning