Abstract:
:The "M" variant of the encephalomyocarditis (EMC) virus causes a diabetes-like disease in some, but not all, strains of mice. The genetic basis for either resistance or susceptibility to the diabetogenic effect of the virus is not known. After infection with EMC, C57BL/6 mice seldom develop hyperglycemia and the insular lesions are subtle. To explore the possible effects of metabolic influences on the viral susceptibility of the islets, we studied C57BL/6 mice that were carriers of the ob gene. After virus inoculation, obese homozygous C57BL/6-ob/ob mice consistently developed hyperglycemia during the acute stages of infection, whereas nonobese littermates did not. Infection induced more severe lesions in the pancreatic islets of obese mice than in islets of the lean littermates. These studies suggest that the functional activity of the beta-cells influences the severity of the viral injury to the beta-cell, and the consequent occurrence of diabetes.
journal_name
Diabetesjournal_title
Diabetesauthors
D'Andrea BJ,Wilson GL,Craighead JEdoi
10.2337/diab.30.5.451subject
Has Abstractpub_date
1981-05-01 00:00:00pages
451-4issue
5eissn
0012-1797issn
1939-327Xjournal_volume
30pub_type
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