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

Niklasson, B ; Samsioe, A ; Blixt, M ; Sandler, S ; Sjöholm, A ; Lagerquist, E ; Lernmark, Åke LU orcid and Klitz, W (2006) In Diabetologia 49(9). p.2192-2199
Abstract
AIMS/HYPOTHESIS: 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. MATERIALS AND METHODS: 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... (More)
AIMS/HYPOTHESIS: 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. MATERIALS AND METHODS: 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. RESULTS: 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 w (Less)
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author
; ; ; ; ; ; and
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Diabetes, Fetal programming, Ljungan virus, Mouse model, Stress, Type 2 diabetes
in
Diabetologia
volume
49
issue
9
pages
2192 - 2199
publisher
Springer
external identifiers
  • scopus:33746695448
  • pmid:16821045
ISSN
1432-0428
DOI
10.1007/s00125-006-0339-8
language
English
LU publication?
no
id
95874882-14f8-4cfc-b2e4-5692be23527d (old id 1136276)
date added to LUP
2016-04-01 11:46:08
date last changed
2022-03-28 02:48:09
@article{95874882-14f8-4cfc-b2e4-5692be23527d,
  abstract     = {{AIMS/HYPOTHESIS: 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. MATERIALS AND METHODS: 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. RESULTS: 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 w}},
  author       = {{Niklasson, B and Samsioe, A and Blixt, M and Sandler, S and Sjöholm, A and Lagerquist, E and Lernmark, Åke and Klitz, W}},
  issn         = {{1432-0428}},
  keywords     = {{Diabetes; Fetal programming; Ljungan virus; Mouse model; Stress; Type 2 diabetes}},
  language     = {{eng}},
  number       = {{9}},
  pages        = {{2192--2199}},
  publisher    = {{Springer}},
  series       = {{Diabetologia}},
  title        = {{Prenatal viral exposure followed by adult stress produces glucose intolerance in a mouse model.}},
  url          = {{http://dx.doi.org/10.1007/s00125-006-0339-8}},
  doi          = {{10.1007/s00125-006-0339-8}},
  volume       = {{49}},
  year         = {{2006}},
}