Boquist L, Lorentzon R
Diabete Metab. 1980 Mar;6(1):55-8.
The initial hyperglycemia in alloxan-treated mice was decreased by adrenalectomy and hypophysectomy, and abolished by occlusion of the hepatic blood flow for 5 min. or treatment with insulin after alloxan injection. No effect on the initial hyperglycemic response to alloxan was found in mice pretreated with phentolamine, or in those given alloxan after sham operation or after removal of ligatures for temporary occlusion of hepatic artery and portal vein. The concentrations of serum insulin and liver glycogen were decreased one and four hours after alloxan injection. The initial hyperglycemia is believed to be due to inhibition of insulin secretion by the B-cells and to the mobilization of glycogen from the liver. Pituitary and adrenocortical activity may contribute to this hyperglycemia. The origin of the hypoglycemic phase does not seem to be pancreatic, but may be hepatic.
用四氧嘧啶处理的小鼠,其最初的高血糖症在肾上腺切除和垂体切除后有所降低,并在肝血流阻断5分钟或四氧嘧啶注射后用胰岛素治疗时被消除。在用酚妥拉明预处理的小鼠中,或在假手术或拆除用于暂时阻断肝动脉和门静脉的结扎线后给予四氧嘧啶的小鼠中,未发现对四氧嘧啶的初始高血糖反应有影响。四氧嘧啶注射后1小时和4小时,血清胰岛素浓度和肝糖原浓度降低。最初的高血糖症被认为是由于β细胞胰岛素分泌受到抑制以及肝脏糖原的动员。垂体和肾上腺皮质活动可能导致这种高血糖症。低血糖期的起源似乎不是胰腺性的,而可能是肝脏性的。