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Patients with severe phenotypes can present in infancy with hypoglycemia and lactic acidosis

intrahepatic factors including hypoxia, lipotoxicity, IR, endoplasmic reticulum (ER) stress, oxidative stress, and mitochondrial dysfunction, as well as extrahepatic factors, such as dysregulated adipokine secretion from dysfunctional adipose tissue (e.g., low adiponectin and high leptin levels), and dysbiosis of gut microbiota, leading to translocation of endotoxins and pathogen-associated molecular patterns (PAMPs) from the portal vein to the liver, contribute to a low-grade, but chronic inflammation, which is orchestrated by a large array of pro-inflammatory mediators [14]

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