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This Article Full Text Full Text (PDF) All Versions of this Article: 581/2/873    most recent jphysiol.2006.126573v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Knight, B. S. Articles by Lye, S. J. Search for Related Content PubMed PubMed Citation Articles by Knight, B. S. Articles by Lye, S. J. Related Collections Integrative Related Article

¹ Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5, CanadaDepartments of
² Physiology
³ Obstetrics & Gynaecology, University of Toronto, Toronto, Ontario M5S 1A8, Canada
⁴ School of Women's and Infants' Health, The University of Western Australia, Perth, WA 6008, Australia

The objective of this study was to characterize offspring responses to maternal dietary restriction (DR) in two phylogenetically distant strains of mice: A/J and C57BL/6J (B6). Pregnant mice were fed 100% or 70% of ad libitum between 6.5 and 17.5 days (d) gestation. Offspring were fed 100% ad libitum postweaning. All comparisons were made to strain and sex matched controls. Male DR-B6 offspring initially grew slower than controls; however, by 77d and 182d they were significantly heavier (P < 0.05). Further, they had an increase percentage fat mass (+70%, P < 0.01) by 182d and were glucose intolerant at both 80d (P < 0.001) and 186d (P < 0.05). In contrast, weight, %Fat mass and glucose tolerance in DR-A/J males during postnatal life were not different from controls. Female DR-B6 mice showed catch-up growth during the first 77d of life; however, their weight, %Fat mass and glucose tolerance were not different from controls at 80d and 186d. Although female DR-A/J were heavier than controls at 182d (P < 0.05), their %Fat mass and glucose tolerance were not different from controls at 182d and 186d. The observed strain and sex differences offer a unique opportunity to begin to define gene–environment interactions that contribute to developmental origins of health and disease.

(Received 13 December 2006; accepted after revision 5 March 2007; first published online 8 March 2007)
Corresponding author S. Lye: 850–600 University Avenue, Toronto, Ontario M5G 1X5, Canada.   Email lye{at}mshri.on.ca

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