Lombardi B
Am J Pathol. 1976 Sep;84(3):633-48.
Choline deficiency enhances greatly the pancreatotoxicity of DL-ethionine. Mice fed DL-ethionine with a choline-deficient diet develop a fatal acute hemorrhagic pancreatic necrosis with fat necrosis (AHPN) in 5 days. Induction of the AHPN is completely prevented by dietary methionine and drastically reduced by dietary methionine and drastically reduced by dietary choline. The amount of proteins, carbohydrates, and fat in the diet influences its consumption by the animals and thus the severity of the pancreatic pathology. The histogenesis of the process is characterized by widespread alterations of the membranous organelles of the acinar cells, especially the endoplasmic reticulum and the zymogen granules. The onset of the hemorrhagic necrosis of the pancreas is due to an endogenous intraparenchymal activation of the zymogenic proteases, including proelastase. The new experimental model of AHPN appears to mimic very closely the clinical course, the anatomic pathologic lesions, and the postulated pathogenesis of the corresponding human disease.
胆碱缺乏会极大地增强 DL-乙硫氨酸的胰腺毒性。用缺乏胆碱的饮食喂养 DL-乙硫氨酸的小鼠，5 天内会发展为致命的急性出血性胰腺坏死伴脂肪坏死（AHPN）。饮食中的蛋氨酸可完全预防 AHPN 的诱导，而饮食中的胆碱可显著降低其发生率。饮食中蛋白质、碳水化合物和脂肪的含量会影响动物的摄入量，进而影响胰腺病理的严重程度。该过程的组织发生学特征是腺泡细胞的膜性细胞器广泛改变，尤其是内质网和酶原颗粒。胰腺出血性坏死的发生是由于包括前弹性蛋白酶在内的酶原性蛋白酶在实质内的内源性激活。新的 AHPN 实验模型似乎非常接近相应人类疾病的临床病程、解剖病理病变和推测的发病机制。
