Virji M A, Rao K N
Am J Pathol. 1985 Jan;118(1):162-7.
In mice fed a choline-deficient diet containing 0.5% DL-ethionine (CDE) profound hypoglycemia develops, as do signs of shock, and the mice die of acute hemorrhagic pancreatitis (AHP). When fed a choline-supplemented diet containing 0.5% DL-ethionine (CSE), however, the mice have a chronic nonhemorrhagic pancreatitis with focal necrosis, do not show symptoms of shock, and survive. For investigation of the mechanism of hypoglycemia and the onset of shock in AHP, serum and pancreatic insulin and glucagon contents, serum glucose levels, and the morphologic characteristics of pancreatic islets were evaluated in mice fed laboratory Chow (LC); a choline-supplemented (CS) diet; a choline-deficient (CD) diet; or the CSE and CDE diets for 1, 2, or 3 days. The results indicate that onset of shock in animals with AHP may be due to hypoglycemia resulting from abnormal release of glucoregulatory hormones and their inability to maintain glucose output from liver and/or caused by active proteinases released from necrotic pancreas.
在喂食含0.5% DL-乙硫氨酸的胆碱缺乏饮食（CDE）的小鼠中，会出现严重低血糖，以及休克症状，小鼠死于急性出血性胰腺炎（AHP）。然而，当喂食含0.5% DL-乙硫氨酸的胆碱补充饮食（CSE）时，小鼠会患慢性非出血性胰腺炎并伴有局灶性坏死，不出现休克症状，并存活下来。为了研究AHP中低血糖和休克发作的机制，对喂食实验室普通饲料（LC）、胆碱补充（CS）饮食、胆碱缺乏（CD）饮食或CSE和CDE饮食1、2或3天的小鼠的血清和胰腺胰岛素及胰高血糖素含量、血清葡萄糖水平以及胰岛的形态特征进行了评估。结果表明，患有AHP的动物休克发作可能是由于葡萄糖调节激素异常释放导致低血糖，以及它们无法维持肝脏的葡萄糖输出和/或由坏死胰腺释放的活性蛋白酶引起的。
