Pathogenesis

Pathogenesis information of NAFLD is manually extracted from research articles.

Disease pathway of NAFLD (Kyoto Encyclopedia of Genes and Genomes)

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     Insulin resistance
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Path ID Pathogenesis Other Terms Description Reference (PMIDs)
P05 Hepatic lipid accumulation Fat metabolism; Lipotoxicity; Lipid accumulation; Lipid metabolism; Hepatocyte insulin resistance; Endoplasmic Reticulum Stress; Mitochondrial Dysfunction Net hepatic TAG accumulation is the result of hepatic lipid supply and demand. The FA transporters (FATP2 and FATP5) and the cluster of differentiation 36 (CD36) facilitate hepatocyte FFA uptake. Studies have reported conflicting findings on the expression patterns of FATP2 and CD36 in humans with steatosis and NASH. An inverse association between hepatic FATP5 messenger RNA expression and histologic changes in NAFLD, including ballooning and fibrosis, suggesting reduced FATP5-mediated TAG accumulation during NASH progression; Increased triglyceride concentration is an epiphenomenon which happens simultaneously with toxic metabolites generation, lipotoxicity and liver injury; DNL, namely, the conversion of acetyl-CoA over malonyl-CoA via acetyl coenzyme A carboxylase (ACC) and finally to palmitate, was independently associated with hepatic TAG in individuals with NAFLD. 33220492; 26823198; 31602526; 24316260; 18072723