Research

Hormonal

In nonalcoholic fatty liver disease (NAFLD), hepatic de novo fatty acid synthesis and uptake are up-regulated (increased ACC1, FAS, SREBP-1c, ADRP) despite existing fatty acid accumulation, driven by a failure of negative feedback regulation.

In NAFLD, the body's normal ability to shut down fat production when fat stores are high is broken. Instead of turning off synthesis, the liver continues to produce and take up fatty acids actively. This suggests that simply reducing dietary fat may not be sufficient if the underlying hormonal regulation (insulin/SREBP-1c) is not addressed.

GoodSupportsHIGH confidence
In NAFLD, although fatty acids accumulated in hepatocytes, their de novo synthesis and uptake were up-regulated in association with increased expression of ACC1, FAS, SREBP-1c, and ADRP.
Motoyuki Kohjima et al. · International Journal of Molecular Medicine · 2007

Why this rating

Human biopsy samples (n=26) with statistical significance (p<0.05) for gene expression changes.

Source

Re-evaluation of fatty acid metabolism-related gene expression in nonalcoholic fatty liver disease

Motoyuki Kohjima et al. · International Journal of Molecular Medicine · 2007

DOI 10.3892/ijmm.20.3.351

mechanism_only · n=36Cited 525×
Read the paper
DOI resolved against Crossref · corpus check 2026-06-10

This is one finding among thousands. Every one is graded and traced to its source, so you can see what the evidence actually supports. Browse the research →