Dysregulated transmethylation leading to hepatocellular carcinoma compromises redox homeostasis and glucose formation

ConclusionGlucose precursor flux away from glucose formation towards pathways that regulate redox status increase in the liver. Moreover, synthesis and scavenging of NAD+ are both impaired resulting in reduced concentrations. This metabolic program blunts an increase in methyl donor availability, however, biosynthetic pathways underlying HCC are activated.
Source: Molecular Metabolism - Category: Endocrinology Source Type: research