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.
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.
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
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