Summary
To study the mechanism of hyperinsulinism and glucose intolerance in liver disease,
insulin removal rate by liver and muscle, glucose uptake by muscle and insulin secretion
from ncreas were measured using the perfusion in rats with injured liver induced by
carbon tetrachloride (liver injury rat).
In the perfused liver, insulin removal rate of liver injury rat decreased to 62 %
of that of normal rat, but it did not alter in the perfused muscle. Insulin response
to arginine by the perfused pancreas of liver injury rat was similar to that of normal
rat. Before insulin infusion, glucose uptake by the perfused muscle was similar in
liver injury rat and normal rat. In contrast, during insulin infusion, glucose uptake
by the perfused muscle was 1.5 times higher in liver injury rat than in normal rat.
These results suggested that the peripheral hyperinsulinism was solely due to decreased
hepatic insulin degradation, but not hypersecretion of insulin from pancreas and furthermore,
might suggest that the insulin resistance was related to appearance of biologically
inactive endogenous insulin, because of exogenous insulin completely acting on peripheral
target tissue.
Key-Words:
Liver Disease
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Hyperinsulinism
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Insulin Resistance
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Liver Perfusion
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Muscle Perfusion
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Pancreas Perfusion
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Insulin Degradation
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Glucose Uptake
