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Energy balance

Mitochondrial fatty acid oxidation capacity in NAFLD is impaired or maximally activated, leading to compensatory up-regulation of peroxisomal and microsomal oxidation pathways.

The liver tries to burn off excess fat through multiple pathways (mitochondrial, peroxisomal, microsomal). In NAFLD, mitochondrial entry (CPT1a) is restricted, but other oxidation pathways are up-regulated to compensate. This suggests that simply 'boosting mitochondrial function' might not address the root cause if the regulatory bottleneck (CPT1a/SREBP-1c) remains.

GoodQualifiesHIGH confidence
Fatty acid oxidation-related genes, LCAD, HADHα, UCP2, ACOX, BOX, CYP2E1, and CYP4A11, were all overexpressed, indicating that oxidation was enhanced in NAFLD, whereas the expression of CTP1a and PPARα was decreased.
Motoyuki Kohjima et al. · International Journal of Molecular Medicine · 2007

Why this rating

Human biopsy samples with statistically significant changes in multiple oxidation genes.

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×
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DOI resolved against Crossref · corpus check 2026-06-10

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