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Loss of PPAR function in hepatocytes initiates DNA hypermethylation of genes related to fatty acid, bile acid, and steroid hormone receptors, including PPAR, leading to progression of disease [339]

5 Plasma concentrations ketone-bodies, glucose, glucagon, lipids, insulin, leptin, and liver inflammation markers

(2019) Methionine is a metabolic dependency of tumor-initiating cells, Nat

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[166] demonstrated that hepcidin overexpression in animal models of hepatic steatosis results in attenuation of steatosis, indicating that patients with both iron overload and hepatic steatosis may benefit from hepcidin-based therapy