Abstract
The dynamics of glucose movement across perfused livers were assessed in carbon tetrachloride (CCl 4)-injured rats. Rats were given CCl 4 for 8 weeks and became glucose intolerant and hyperinsulinemic. The fasted rat liver was cyclically perfused with 4 mM lactate and various concentrations (0-20 mM) of glucose for 20 min. In the CCl 4-injured liver, net glucose output was less suppressed at high glucose levels than in the normal liver (147 ± 70 vs 18 ± 10 μmol at 20 mM glucose, P < 0.05). Deposition of the carbon from [ 14C]glucose into glycogen was stimulated at high glucose levels and was markedly reduced in the CCl 4-injured liver compared to the normal liver (0.58 ± 0.33 μmol vs 1.44 ± 0.20 μmol at 20 mM, P < 0.01). Conversion of [ 14C]lactate to [ 14C]glucose was not different between the CCl 4-injured and the normal liver at each glucose level. Deposition of the carbon from [ 14C]lactate into glycogen in the CCl 4-injured liver was larger than that in the normal liver at 0 mM glucose (0.82 ± 0.15 μmol vs 0.32 ± 0.06 μmol, P < 0.01), but was similar to the normal at 20 mM glucose. In the CCl 4-injured liver, utilization of exogenous glucose was impaired at high glucose levels, and gluconeogenetic activity was not impaired at low glucose levels. These changes in the hepatic glucose metabolism seem to account for postprandial hyperglycemia without fasting hypoglycemia associated with liver diseases.
Published Version
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