Research

Mixed

Systemic insulin resistance drives hepatic steatosis in NAFLD by increasing adipose lipolysis and hepatic de novo lipogenesis, while specific saturated fatty acids (like palmitate) cause lipotoxicity, ER stress, and hepatocyte apoptosis, which triggers innate and adaptive immune responses leading to NASH and fibrosis.

NAFLD/NASH is driven by insulin resistance and toxic lipid accumulation (lipotoxicity), not just 'fat in the liver.' Managing insulin sensitivity and reducing saturated fat intake may help, but genetic factors and immune system activation also play critical roles in progression to liver damage.

GoodSupportsHIGH confidence
Systemic insulin resistance is a major driver of hepatic steatosis in NAFLD. Lipotoxicity of accumulated lipids along with activation of the innate immune system are major drivers of NASH. Lipid-induced sublethal and lethal stress culminates in the activation of inflammatory processes... Innate and adaptive immune mechanisms... are central drivers of inflammation that recognize damage- and pathogen-associated molecular patterns and contribute to the progression of the inflammatory cascade.
Gopanandan Parthasarathy et al. · Hepatology Communications · 2020

Why this rating

Review of multiple human and animal studies, multiomics, and genetic data; high quality but observational/mechanistic.

Source

Pathogenesis of Nonalcoholic Steatohepatitis: An Overview

Gopanandan Parthasarathy et al. · Hepatology Communications · 2020

DOI 10.1002/hep4.1479

narrative_reviewCited 421×
Read the paper
DOI resolved against Crossref · corpus check 2026-06-10

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