Prenatal viral exposure followed by adult stress produces glucose intolerance in a mouse model

Bo NiklassonWilliam Klitz


It has been suggested that the uterine environment may influence metabolic disease occurring later in adult life, and that adult stress may promote disease outcome. Using a mouse model, we tested whether in utero exposure to Ljungan virus (LV) followed by adult exposure to stress produces diabetes. The influence of the timing of viral exposure over the course of pregnancy was also tested. Pregnant CD-1 mice were exposed i.p. to LV on pregnancy days 4, 8, 12 or 17. Adult male mice from these pregnancies were stressed by being kept in shared cages. Stress only, LV exposure in utero only, and no-stress/no virus exposure groups were also followed. Outcome variables included bodyweight, epididymal fat weight, baseline glucose, glucose tolerance tests (60 and 120 min) and serum insulin. We demonstrated that male mice developed a type 2-like diabetes, including obesity, as adults if infected during pregnancy with LV. Diabetes at the age of 11 weeks was more severe in mice whose mothers were infected earlier than in those whose mothers were infected later in pregnancy. Only animals infected in utero and kept under stress developed diabetes; infection or stress alone did not cause disease. This work demonstrates that a type 2 diabetes-l...Continue Reading


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Related Concepts

Blood Glucose
Diabetes Mellitus
Diabetes Mellitus, Non-Insulin-Dependent
Insulin B Chain
Picornaviridae Infections
Pregnancy Complications, Infectious
Metabolic Stress Response
Impaired Glucose Tolerance