Weaver C, Sorenson R L, Kaung H L
Diabetes. 1986 Jan;35(1):13-9. doi: 10.2337/diab.35.1.13.
Murine copper deficiency induced by diet and supplemented with a copper chelator is known to produce a progressive atrophy of pancreatic acinar tissue largely replaced by noninflammatory lipomatosis, while the ductal and endocrine systems appear to remain unaffected. The islets were studied morphologically and physiologically in animals rendered copper deficient by diet and supplemented with D-penicillamine. Using immunohistochemistry, the distribution of islet cell types from copper-deficient animals exhibited a normal cellular complement for A-, B-, D-, and PP-cells. Ultrastructural analysis showed the islet tissue remains normal in appearance during the course of the metal-deficient state. Physiologic data based on the response of islets to a low- and high-glucose load in perfused, isolated pancreata as well as intravenous glucose tolerance tests indicated that insulin-secreting B-cells were functionally normal. Because of the accessibility of islets enhanced by atrophy of acini, this model may be adopted for the isolation of viable islets and for in situ physiologic studies of islet hormone secretion.
已知通过饮食诱导并补充铜螯合剂导致的小鼠铜缺乏会使胰腺腺泡组织逐渐萎缩，大部分被非炎性脂肪瘤替代，而导管和内分泌系统似乎未受影响。对通过饮食造成铜缺乏并补充D-青霉胺的动物的胰岛进行了形态学和生理学研究。使用免疫组织化学方法，来自铜缺乏动物的胰岛细胞类型分布显示A细胞、B细胞、D细胞和PP细胞的细胞组成正常。超微结构分析表明，在金属缺乏状态过程中，胰岛组织外观保持正常。基于灌注、分离胰腺中胰岛对低葡萄糖负荷和高葡萄糖负荷的反应以及静脉葡萄糖耐量试验的生理学数据表明，分泌胰岛素的B细胞功能正常。由于腺泡萎缩增强了胰岛的可及性，该模型可用于分离活的胰岛以及进行胰岛激素分泌的原位生理学研究。
