Degradation of insulin in perfused liver and skeletal muscle and insulin secretion in perfused pancreas of liver injury rat.
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 pancreas 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.
D000818:Animals; D002252:Carbon Tetrachloride Poisoning / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism; D006207:Half-Life; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism* / Q000494:pharmacology; D007700:Kinetics; D008099:Liver / Q000378:metabolism*; D008297:Male; D009132:Muscles / Q000187:drug effects / Q000378:metabolism*; D010179:Pancreas / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D007328:Insulin; D005947:Glucose