{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T18:39:55Z","timestamp":1792521595913,"version":"4.5.0"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","license":[{"start":{"date-parts":[[2020,10,30]],"date-time":"2020-10-30T00:00:00Z","timestamp":1604016000000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatology"],"published-print":{"date-parts":[[2020,11]]},"abstract":"<jats:sec>\n            <jats:title>Background and Aims<\/jats:title>\n            <jats:p>Glycogen storage disease (GSD) type 1a is an inborn error of metabolism caused by defective glucose\u20106\u2010phosphatase catalytic subunit (G6PC) activity. Patients with GSD 1a exhibit severe hepatomegaly due to glycogen and triglyceride (TG) accumulation in the liver. We have shown that the activity of carbohydrate response element binding protein (ChREBP), a key regulator of glycolysis and <jats:italic toggle=\"yes\">de novo<\/jats:italic> lipogenesis, is increased in GSD 1a. In the current study, we assessed the contribution of ChREBP to nonalcoholic fatty liver disease (NAFLD) development in a mouse model for hepatic GSD 1a.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results<\/jats:title>\n            <jats:p>Liver\u2010specific <jats:italic toggle=\"yes\">G6pc<\/jats:italic>\u2013knockout (L\u2010<jats:italic toggle=\"yes\">G6pc<\/jats:italic>\n                                 <jats:sup>\u2212\/\u2212<\/jats:sup>) mice were treated with adeno\u2010associated viruses (AAVs) 2 or 8 directed against short hairpin ChREBP to normalize hepatic ChREBP activity to levels observed in wild\u2010type mice receiving AAV8\u2013scrambled short hairpin RNA (shSCR). Hepatic ChREBP knockdown markedly increased liver weight and hepatocyte size in L\u2010<jats:italic toggle=\"yes\">G6pc<\/jats:italic>\n                                 <jats:sup>\u2212\/\u2212<\/jats:sup> mice. This was associated with hepatic accumulation of G6P, glycogen, and lipids, whereas the expression of glycolytic and lipogenic genes was reduced. Enzyme activities, flux measurements, hepatic metabolite analysis and very low density lipoprotein (VLDL)\u2010TG secretion assays revealed that hepatic ChREBP knockdown reduced downstream glycolysis and <jats:italic toggle=\"yes\">de novo<\/jats:italic> lipogenesis but also strongly suppressed hepatic VLDL lipidation, hence promoting the storage of \u201cold fat.\u201d Interestingly, enhanced VLDL\u2010TG secretion in shSCR\u2010treated L\u2010<jats:italic toggle=\"yes\">G6pc<\/jats:italic>\n                                 <jats:sup>\u2212\/\u2212<\/jats:sup> mice associated with a ChREBP\u2010dependent induction of the VLDL lipidation proteins microsomal TG transfer protein and transmembrane 6 superfamily member 2 (TM6SF2), the latter being confirmed by ChIP\u2010qPCR.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>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\u2010TG 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.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.31198","type":"journal-article","created":{"date-parts":[[2020,2,21]],"date-time":"2020-02-21T15:35:05Z","timestamp":1582299305000},"page":"1638-1653","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":37,"title":["Hepatic Carbohydrate Response Element Binding Protein Activation Limits Nonalcoholic Fatty Liver Disease Development in a Mouse Model for Glycogen Storage Disease Type 1a"],"prefix":"10.1097","volume":"72","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7246-8305","authenticated-orcid":false,"given":"Yu","family":"Lei","sequence":"first","affiliation":[{"name":"Department of Pediatrics,University Medical Center Groningen,University of Groningen,Groningen,the 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Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5391-8024","authenticated-orcid":false,"given":"Aycha","family":"Bleeker","sequence":"additional","affiliation":[{"name":"Department of Pediatrics,University Medical Center Groningen,University of Groningen,Groningen,the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henk","family":"Wolters","sequence":"additional","affiliation":[{"name":"Department of Pediatrics,University Medical Center Groningen,University of Groningen,Groningen,the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0066-3720","authenticated-orcid":false,"given":"Justina C.","family":"Wolters","sequence":"additional","affiliation":[{"name":"Department of Pediatrics,University Medical Center Groningen,University of Groningen,Groningen,the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brenda S.","family":"Hijmans","sequence":"additional","affiliation":[{"name":"Department of Pediatrics,University Medical Center Groningen,University of Groningen,Groningen,the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2713-049X","authenticated-orcid":false,"given":"Theo H.","family":"van Dijk","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine,University Medical Center Groningen,University of Groningen,Groningen,the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6210-9974","authenticated-orcid":false,"given":"Rachel","family":"Thomas","sequence":"additional","affiliation":[{"name":"Dutch Molecular Pathology Center,Faculty of Veterinary Medicine,Utrecht University,Utrecht,the 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