Blood galactose clearance after an intravenous galactose load has been wide
ly used for years as an index of liver function. We developed a noninvasive
[C-13]galactose breath test, which explores galactose oxidative metabolism
; this test is well correlated with liver fibrosis in patients with chronic
Viral hepatitis. The goal of this study was to evaluate the influence of n
onhepatic factors such as diabetes and ethanol on whole-body galactose clea
rance (measured as the serum galactose elimination capacity test) and oxida
tive metabolism (measured as the [C-13]galactose-induced breath (CO2)-C-13
production) in rats. Acute ethanol administration induced a significant dec
rease of galactose clearance and (CO2)-C-13 production. There was a signifi
cant correlation between the amount of ethanol given and the inhibition of
galactose metabolism (R-2 = 0.72, p < 0.0001). In streptozotocin-induced di
abetic rats, the [C-13]galactose-induced breath (CO2)-C-13, production was
significantly reduced (p < 0.0001) and normalized by insulin treatment. How
ever, diabetes did not decrease whole-body galactose clearance, indicating
an isotopic dilution of [C-13]glucose produced from [C-13]galactose metabol
ism into the enlarged glucose pool. These results must be taken into accoun
t when using the [C-13]galactose breath test as a quantitative liver functi
on test.