Ketogenesis mitigates metabolic dysfunction-associated steatotic liver disease through mechanisms that extend beyond fat oxidation.

Compared with control mice receiving scrambled ASO, the livers of chow-fed ketogenesis-insufficient mice exhibited an 80% ± 24% diminution in total fat oxidation (Student’s t test, P < 0.001), a 76% ± 24% impairment in REs generated from β-oxidation, and a strong trend toward a decrease in total RE production rate (39% ± 23% Student’s t test, P = 0.056), despite a trend toward a 70% ± 23% increase in TCA cycle–sourced REs (Student’s t test, P = 0.1108) ( Figure 8, B and C ).

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