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This Article Full Text Full Text (PDF) All Versions of this Article: 579/3/643    most recent jphysiol.2006.122101v2 jphysiol.2006.122101v1 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 Nijland, M. J. Articles by Cox, L. A. Search for Related Content PubMed PubMed Citation Articles by Nijland, M. J. Articles by Cox, L. A. Related Collections Molecular and Genomic

¹ Department of Obstetrics and Gynecology and Center for Pregnancy and Newborn Research, University of Texas Health Science Center, San Antonio, TX, USA
⁴ Department of Genetics
² South west National Primate Research Center
³ Division of Veterinary Resources, South west Foundation for Biomedical Research, San Antonio, TX, USA

Developmental programming is defined as the process by which gene–environment interaction in the developing organism leads to permanent changes in phenotype and function. Numerous reports of maternal nutrient restriction during pregnancy demonstrate altered renal development. Typically this alteration manifests as a reduction in the total number of glomeruli in the mature kidney of the offspring, and suggests that predisposition to develop chronic renal disease may include an in utero origin. In a previous study, we defined the transcriptome in the kidney from fetuses of control (CON, fed ad libitum) and nutrient-restricted (NR, fed 70% of CON starting at 0.16 gestation (G)) pregnancies at half-way through gestation (0.5G), and established transcriptome and morphological changes in NR kidneys compared to CON. One goal of the present study was to use transcriptome data from fetal kidneys of CON and NR mothers at 0.5G with histological data to identify the molecular mechanisms that may regulate renal development. A second goal was to identify mechanisms by which NR elicits its affect on fetal baboon kidney. We have used an end-of-pathway gene expression analysis to prioritize and identify key pathways regulating the 0.5G kidney phenotype in response NR. From these data we have determined that the mammalian target of rapamycin (mTOR) signalling pathway is central to this phenotype.

(Received 30 September 2006; accepted after revision 20 December 2006; first published online 21 December 2006)
Corresponding author L. A. Cox: Department of Genetics, South west National Primate Research Center, South west Foundation for Biomedical Research, 7620 NW Loop 410, San Antonio, TX 78227-5301 USA. Email: lcox{at}darwin.sfbr.org

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