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Interestingly, the researchers found that lymphocytes in these patients had elevated levels of glutathione, which they hypothesize is a desperate, inadequate compensatory response by the cells trying to survive the relentless oxidative avalanche

Eur J Gastroenterol Hepatol 2014;26:137-145

Deficiency of lipin-1, a lipid metabolism-related molecule, downregulates FAO by inhibiting PGC-1/PPAR-mediated CPT1A/hepatic nuclear factor 4 alpha (HNF4) signaling and upregulates sterol-regulatory element binding protein (SREBP) to promote fat synthesis, thereby causing renal tubular epithelial cell damage and exacerbating fibrosis [52]