Mongrel dogs were prepared by cholecystectomy, ligation of the lesser pancreatic duct, and insertion of modified Thomas cannulas into the stomach and duodenum. When the dogs had recovered from surgery, studies were performed on them, conscious and unanesthetized after an overnight fast. The common bile duct was catheterized through the opened duodenal cannula for collection of hepatic bile. Bile flow was stabilized by the intravenous infusion of sodium taurocholate. After 2 hr of taurocholate infusion, insulin was added to the infusion and continued for the duration of the experiment. Glucose was administered intravenously during the first 120 min of insulin administration to maintain euglycemia; then the glucose was discontinued. The intravenous infusion of insulin during euglycemia maintained by glucose infusion caused a significant increase in bile flow and a decrease in bile salt concentration, but no change in bile salt output. There was a decrease in cholesterol concentration and output and in phospholipid concentration, but no significant change in phospholipid output. When glucose infusion was discontinued and hypoglycemia occurred, there was a further significant increase in bile flow, but no other change. These studies demonstrate that the choleretic action of insulin is not dependent upon hypoglycemia and that intravenously administered insulin may cause increased bile secretion without increase in serum glucagon concentration. These experiments also confirm that insulin choleresis may be associated with a decline in cholesterol output.
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