Table of Contents Author Guidelines Submit a Manuscript
Experimental Diabetes Research
Volume 2011 (2011), Article ID 171376, 5 pages
Research Article

Increased Placental Glucose Transport Rates in Pregnant Mice Carrying Fetuses with Targeted Disruption of Their Placental-Specific Igf2 Transcripts Are Not Associated with Raised Circulating Glucose Concentrations

1Department of Paediatrics, University of Cambridge, Box 116, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK
2Department of Medicine, University of Cambridge, Cambridge CB2 0QQ, UK
3Institute of Metabolic Science, University of Cambridge, Cambridge CB2 0QQ, UK
4M.R.C. Epidemiology Unit, Addenbrooke's Hospital, Cambridge CB2 0QQ, UK
5Babraham Institute, Babraham CB22 3AT, UK
6Centre for Trophoblast Research, University of Cambridge, Cambridge CB2 3EG, UK
7Department of Obstetrics & Gynaecology, University of Cambridge, Cambridge CB2 0SW, UK

Received 6 September 2010; Accepted 13 January 2011

Academic Editor: F. Chiarelli

Copyright © 2011 Clive J. Petry et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


At the beginning of the third week of pregnancy, mouse fetuses with targeted disruption of their paternally-transmitted insulin-like growth factor 2 gene placental-specific transcripts have growth-restricted placentas but normal body weights due to upregulated placental nutrient transport. We assessed whether increased placental glucose transport rates were associated with raised maternal glucose concentrations by performing intraperitoneal glucose tolerance tests (ipGTT) in pregnant mice carrying knockout pups and comparing them with mice carrying genotype-matched phenotypically wild type pups. Mean ± SD body weights of affected pups were 95 ± 8% of control values at e16 and 73 ± 7% at e18. There were no differences in areas under the maternal ipGTT curves at either e16 (mean ± SD being 99.0 ± 9.1% of control values; P=.9) or e18 (91.4 ± 13.4%; P=.3), suggesting that effects on transplacental glucose transport in these mice are not mediated through changes in maternal glucose concentrations.