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.
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.
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
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