Glucose intolerance and pancreatic endocrine dysfunction in dogs with obstructive jaundice.
Mechanisms involved in pancreatic endocrine disturbances in the presence of obstructive jaundice were studied in mongrel dogs with a ligated bile duct. Slower disappearance rate of glucose (KG) and lower portal insulin responses within ten minutes following intravenous glucose loading were observed in jaundiced dogs than in the controls. Hyperglucagonemia in the portal vein was evident in jaundiced dogs for five weeks. Morphometrical analysis of the beta-cells showed that the volume density of secretory granules decreased in jaundiced dogs. However, in three types of beta-granules, the change of size was observed only in the bar-shaped core granules. The volume density of the rough endoplasmic reticulum increased whereas that of the Golgi apparatus decreased in jaundiced dogs for five weeks. In contrast with beta-cells, alpha-cells revealed no morphological changes in any groups. These findings suggest that the beta-granules fail to mature if there is an inhibition by a blockade of energy-requiring steps such as the ER-Golgi transfer system. Impairment of beta-granules is considered to lead to glucose intolerance. Hyperglucagonemia is probably secondary to abnormal beta-cell function, which causes insulin deficiency and the loss of the relation between alpha-cells and beta-cells.
Obata
H
H
First Department of Surgery, Kyushu University Faculty of Medicine, Fukuoka, Japan.
Koga
A
A
D000818:Animals; D002779:Cholestasis / Q000503:physiopathology*; D003594:Cytoplasmic Granules / Q000378:metabolism; D004285:Dogs; D005260:Female; D005934:Glucagon / Q000097:blood; D005947:Glucose / Q000494:pharmacology*; D005951:Glucose Tolerance Test; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000503:physiopathology* / Q000648:ultrastructure; D008297:Male
D007328:Insulin; D005934:Glucagon; D005947:Glucose