Research

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.

GoodSupportsHIGH confidence
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.
Santhosh Satapati et al. · Journal of Clinical Investigation · 2015

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

mechanism_onlyCited 402×
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DOI resolved against Crossref · corpus check 2026-06-10

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