Energy balance
Elevated hepatic anaplerotic/cataplerotic flux (biosynthetic workload) drives oxidative stress and inflammation in fatty liver by necessitating increased oxidative metabolism.
In fatty liver, the liver's attempt to produce glucose (gluconeogenesis) forces it to burn fuel inefficiently, creating toxic byproducts (ROS) that cause inflammation. Interventions that reduce this biosynthetic workload (like Metformin or genetic suppression of PEPCK) reduce inflammation, suggesting that therapies targeting hepatic glucose production may alleviate liver damage.
induction of biosynthesis through hepatic anaplerotic/cataplerotic pathways is energetically backed by elevated oxidative metabolism and hence contributes to oxidative stress and inflammation during NAFLD.
Why this rating
Strong mechanistic evidence in mice and correlation in human biopsies, though human intervention data is limited to metformin observation.
Source
Mitochondrial metabolism mediates oxidative stress and inflammation in fatty liver
Santhosh Satapati et al. · Journal of Clinical Investigation · 2015
DOI 10.1172/jci82204
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