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1 Department of Obstetrics & Gynaecology, University of Western Ontario, Canadian Institutes of Health Research Group in Fetal and Neonatal Health and Development, Children's Health Research Institute & Lawson Health Research Institute, London, ON, Canada
2 Department of Medicine, University of Western Ontario, Canadian Institutes of Health Research Group in Fetal and Neonatal Health and Development, Children's Health Research Institute & Lawson Health Research Institute, London, ON, Canada
3 Department of Medicine, University of Western Ontario, Canadian Institutes of Health Research Group in Fetal and Neonatal Health and Development, Children's Health Research Institute & Lawson Health Research Institute, London, ON, Canada; Department of Physiology and Pharmacology, University of Western Ontario, Canadian Institutes of Health Research Group in Fetal and Neonatal Health and Development, Children's Health Research Institute & Lawson Health Research Institute, London, ON, Canada
4 Department of Obstetrics & Gynaecology, University of Western Ontario, Canadian Institutes of Health Research Group in Fetal and Neonatal Health and Development, Children's Health Research Institute & Lawson Health Research Institute, London, ON, Canada; Department of Physiology and Pharmacology, University of Western Ontario, Canadian Institutes of Health Research Group in Fetal and Neonatal Health and Development, Children's Health Research Institute & Lawson Health Research Institute, London, ON, Canada
* To whom correspondence should be addressed. E-mail: kyang{at}uwo.ca.
There is increasing evidence that poor early growth confers an increased risk of type 2 diabetes, hypertension, and other features of the metabolic syndrome in later life. It is hypothesized that this may result from poor nutrition during early life exerting permanent effects on the structure and function of key metabolic organ systems. To study the long-term impact of early life under-nutrition on susceptibility to visceral adiposity, we used a rat model of maternal protein restriction (MPR) in which dams were fed a low protein diet (containing 8% instead of 20% protein in the control diet) throughout pregnancy and lactation. MPR offspring were born smaller than controls (offspring of dams on the control diet) and in adulthood developed visceral adiposity. We compared the pattern of gene expression in visceral adipose tissue (VAT) between MPR offspring and controls using Affymetrix Rat Expression Arrays. Of the total number of genes and expressed sequence tags analyzed (15,923 probe sets), 9790 (61.5%) were expressed in VAT. We identified 650 transcripts as differentially expressed by at least 1.5-fold in the VAT of MPR offspring. Gene ontology analysis revealed a global up-regulation of genes involved in carbohydrate, lipid and protein metabolism. A number of genes involved in adipocyte differentiation, angiogenesis and extra-cellular matrix remodeling were also up-regulated. However, in marked contrast to other rodent models of obesity, the expression of a large number of genes associated with inflammation was reduced in this rat model. Therefore, visceral adiposity in this early life programmed rat model is marked by dynamic changes in the transcriptional profile of VAT. Our data provide new insights into the molecular mechanisms that underlie the early life programming of visceral adiposity.
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