Functional alterations in pancreatic beta cells as a factor in virus-induced hyperglycemia in mice.

摘要: Alterations in the functional capacity of pancreatic beta cells appear to contribute coxsackievirus B4-induced, long-term hyperglycemia mice. Mice infected with prototype B4 or its diabetogenic E2 variant were monitored for abnormalities sugar metabolism (by glucose tolerance test), total protein and insulin synthesis intact cells, alterations cell proteins, virus replication. The mice hypoglycemic at 72 h postinfection hyperglycemic 6 weeks. At 8 weeks postinfection, few prototype- but most E2-infected remained hyperglycemic. Total immunoprecipitable decreased during early infection. prototype-infected increased almost level control Although likewise mice, it well below level. Two-dimensional gel electrophoresis revealed disappearance many cellular proteins from very postinfection. Many disappearing reappeared gradually group. Infectious was recovered only Functional impairment these appears be a factor virus-induced hyperglycemia.