Non-alcoholic fatty liver disease alters expression of genes governing hepatic nitrogen conversion.
Peter Lykke EriksenHendrik VilstrupKristoffer RigboltMalte P SuppliMichael SørensenSara HeebøllSanne S VeidalFillip K KnopKaren Louise ThomsenPublished in: Liver international : official journal of the International Association for the Study of the Liver (2019)
NAFLD downregulated the expression of urea cycle-related genes. Downregulation of urea cycle flux-generating CPS1 correlated with the loss of functional capacity for ureagenesis in NASH. On gene level, these changes coincided with an increase in the major ammonia scavenging enzyme GS. The effects seemed related to a fatty liver as such rather than NASH or obesity. The findings support gene regulatory mechanisms involved in the deficient ureagenesis of NAFLD, but it remains unexplained how hepatocyte fat accumulation exerts these effects.
Keyphrases
- poor prognosis
- genome wide
- type diabetes
- metabolic syndrome
- insulin resistance
- adipose tissue
- binding protein
- weight loss
- genome wide identification
- fatty acid
- gene expression
- copy number
- weight gain
- skeletal muscle
- physical activity
- dna methylation
- ionic liquid
- high fat diet induced
- drug induced
- bioinformatics analysis