Experimental non-alcoholic fatty liver disease causes regional liver functional deficits as measured by the capacity for galactose metabolism while whole liver function is preserved.

Comparing early and late NAFLD animals, normalised to their respective control group, late NAFLD animals had significantly lower 18 F-FDGal tracer uptake (p = 0.006), although the difference in fat-corrected tracer uptake and COV did not reach statistical significance (p ≥ 0.12).

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Moreover, the borderline significant results on reduced fat-corrected 18 F-FDGal accumulation in late NAFLD may well be the result of the low number of observations; the group difference visually and numerically seemed convincing.

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