Rapid transient increase of biliary triiodothyronine excretion during short-term infusion of glucose and arginine in rats.

OBJECTIVE

To estimate the excretion of triiodothyronine by bile in groups of rats infused with glucose, arginine or glucose combined with various doses of insulin.

MATERIALS AND METHODS

Groups of about eight male Wistar Olac rats were anesthetized by pentobarbital and thin polyethylene tubings were inserted into bile duct and femoral vein. The bile was collected into pre-weighed glass vials which were changed every hour. The first one hour interval was considered as control and during the second hour the following i.v. infusions were applied: 1. 2.4 ml 30 % glucose; 2. arginine (80 mg/2. 4 ml saline); 3. 2.4 ml 30 % glucose containing 62.5, 125, 250 or 500 mU insulin. In some groups cycloheximide (2.5 mg/kg) or somatostatin (20 microg/kg) were used. The aliquots of bile were treated with beta-glucuronidase/arylsulfatase and the concentration of total (i.e. conjugated plus unconjugated) triiodothyronine was estimated by specific inhouse radioimmunoassay. The results were expressed as ng/hr and the volume of bile was estimated by weighing the previously tared collection vials.

RESULTS

Significant increase of biliary T3 excretion was found during the 60 min infusion of glucose or arginine. However, in fed rats such increase did not continue after the termination of infusion, while in fasted rats the increase was observed still for next 60 min after the infusion. The attempts to further stimulate the excretion of T3 by the addition of small insulin doses (62.5, 125, 250 and 500 mU) to the infused glucose showed inversed effect: by such intervention the increase of T3 was blunted by higher doses, while at lower doses unsignificant increase appeared. The increase of biliary T3 excretion was also blunted by cycloheximide (translation inhibitor) and somatostatin (insulin release inhibitor) both in normal fed and 24 hr fasted rats.

CONCLUSIONS

Short-term i.v. infusion of glucose and arginine resulted in immediate and transient increase of biliary T3 excretion which was inhibited by both the cycloheximide and somatostatin. Taken together with our previous findings, this supports the view on rapid fluctuation of hepatic iodothyronine metabolism as related to preprandial (prevailing effect of gluconeogenetic hormones resulting in preferential formation of rT3) and postprandial period (predominant effect of insulin resulting in preferential formation of T3).