Utsugi T, Kanda T, Tajima Y, Tomono S, Suzuki T, Murata K, Dan K, Seto Y, Kawazu S
2nd Department of Internal Medicine, Gunma University School of Medicine, Maebashi, Japan.
Diabetes Res. 1992;20(4):109-19.
Intraperitoneal inoculation with NDK25, a variant of Encephalomyocarditis (EMC) virus which has been newly cloned from the M variant of EMC virus (EMC-M), caused DBA/2 mice to develop noninsulin-dependent diabetes mellitus. The NDK25-infected mice demonstrated abnormal glucose tolerance from 1 to 3 weeks after inoculation. The infection resulted in mild insulitis and the destruction of pancreatic beta cells at 1 week after inoculation and led to a significant reduction in the insulin content of the pancreas, but there was no ketonuria. The insulin content of the pancreas was recovered considerably from 15 +/- 3 at 1 week to 95 +/- 16 micrograms/g pancreas at 12 weeks, although the latter value was still significantly lower than that of the control mice (P < 0.05). Under microscopy, mild and partial infiltration of mononuclear cells was observed in about half the pancreatic islets only 1 week after inoculation, and then disappeared. Thus, we believe we have established a new model of noninsulin-dependent diabetes mellitus using the NDK25 variant of EMC virus.
用NDK25（一种从脑心肌炎病毒M变种（EMC-M）中新克隆出的变种）进行腹腔接种，会使DBA/2小鼠患上非胰岛素依赖型糖尿病。接种后1至3周，感染NDK25的小鼠表现出异常的葡萄糖耐量。接种后1周，感染导致轻度胰岛炎和胰腺β细胞破坏，并导致胰腺胰岛素含量显著降低，但无酮尿症。胰腺胰岛素含量从1周时的15±3微克/克胰腺大幅恢复至12周时的95±16微克/克胰腺，尽管后者仍显著低于对照小鼠（P<0.05）。在显微镜下，接种后仅1周，约一半的胰岛中观察到轻度单核细胞局部浸润，然后消失。因此，我们相信我们已经利用脑心肌炎病毒的NDK25变种建立了一种新的非胰岛素依赖型糖尿病模型。
