BILE FLOW EXPERIMENTS IN NON‐DIABETIC ANIMALS

Summary Bile flow experiments were performed on 41 non‐diabetic animals. A biliary fistula was created in 19 cases, and ligation of the common bile duct was performed in 22. In 9 of the former animals, the mean postoperative observation period amounted to 27.6 days; the corresponding mean in 11 animals in the latter group was 23.5 days. Quantitative micro‐morphologic analyses were performed in these 20 cases, and the results were compared with those in 17 similarly fed controls. An account is given of the postoperative course in these experiments. Glucose tolerance tests were made before and after the respective interventions. As a rule, the biliary fistula animals exhibited a slightly increased tolerance in comparison to the controls, whereas no change in the tolerance was recorded in the animals with biliary stasis. A distinctly decreased tolerance was, however, recorded in one animal in the former group and in three in the latter, the decrease being greater than in the similarly underfed controls. This decreased tolerance has been interpreted as a result of impaired glycogenesis and glycogenolysis due to liver damage. In the biliary fistula animals, an increased insulin output from the pancreas may have been responsible for the raised glucose tolerance. At autopsy, a more or less severe degree of reduction in the adipose tissue was found in both groups of operated animals. This feature is discussed. It is considered improbable that its cause is decreased absorption of the quantitatively inappreciable dietary fat. It may have been due to a disturbance in lipogenesis, as a result of liver cell damage. An enlargement of the pancreas was observed in both the biliary fistula and the biliary stasis animals. It appeared both in the weight of the organ, and in micromorphologic determination of the parenchyma; significant differences were present in relation to the corresponding values in the control groups. The increase in parenchymal volume, expressed in mm 3 per kg of body weight, amounted to about 60 per cent in comparison to the controls. The mechanism underlying this increase in pancreatic volume is discussed. An increase in the size of the islet tissue was present in both groups, the differences being significant as compared to the values in the control groups. The increase in islet volume, expressed in mm 3 per kg of body weight, amounted to about 100 per cent in relation to the volume in the control groups. The alpha cell incidence was somewhat lower in the biliary fistula animals than in the corresponding control group. In the biliary stasis animals, the alpha cell incidence was the same as in the controls. In all the groups, this incidence was within the normal range of variation.