Yoon J W, Reddi A H
Am J Physiol. 1984 Jan;246(1 Pt 1):C177-9. doi: 10.1152/ajpcell.1984.246.1.C177.
Severe hyperglycemic and hypoinsulinemic mice were selected at 30 and 180 days after infection with the D variant of encephalomyocarditis (EMC) virus. In these animals, although the concentration of calcium and phosphate in serum was not changed, the alkaline phosphatase activity and the rate of mineralization in the proximal tibial epimetaphysis were markedly decreased in the diabetic mice for 30 and 180 days compared with those of the age-matched uninfected animals. Viral specific antigens were not found in these tissues at either earlier or later infection with the virus. It is concluded that endochondral bone formation and mineralization are greatly impaired in EMC virus-induced diabetic mice, and the decreased bone formation and mineralization are not due to the virus-induced tissue damage, but to the persistent metabolic alterations.
在感染脑心肌炎（EMC）病毒D变体30天和180天后，选择严重高血糖和低胰岛素血症小鼠。在这些动物中，虽然血清中钙和磷的浓度没有变化，但与年龄匹配的未感染动物相比，糖尿病小鼠在30天和180天时近端胫骨干骺端的碱性磷酸酶活性和矿化速率明显降低。在这些组织中，无论早期还是晚期感染该病毒，均未发现病毒特异性抗原。得出的结论是，在EMC病毒诱导的糖尿病小鼠中，软骨内骨形成和矿化受到极大损害，骨形成和矿化的减少不是由于病毒诱导的组织损伤，而是由于持续的代谢改变。
