Hindawi Publishing Corporation Journal of Nutrition and Metabolism Volume 2013, Article ID 517384, 11 pages http://dx.doi.org/10.1155/2013/517384 Research Article Timing of Maternal Exposure to a High Fat Diet and Development of Obesity and Hyperinsulinemia in Male Rat Offspring: Same Metabolic Phenotype, Different Developmental Pathways? Graham J. Howie, 1 Deborah M. Sloboda, 1,2 Clare M. Reynolds, 1 and Mark H. Vickers 1 1 Liggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, 2-6 Park Avenue, Graton, Auckland 1010, New Zealand 2 Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada L8S 4L8 Correspondence should be addressed to Mark H. Vickers; m.vickers@auckland.ac.nz Received 11 February 2013; Revised 8 April 2013; Accepted 20 April 2013 Academic Editor: Peter M. Cliton Copyright © 2013 Graham J. Howie et al. his 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. Objective. Ofspring born to mothers either fed an obesogenic diet throughout their life or restricted to pregnancy and lactation demonstrate obesity, hyperinsulinemia, and hyperleptinemia, irrespective of their postweaning diet. We examined whether timing of a maternal obesogenic diet results in diferential regulation of pancreatic adipoinsular and inlammatory signaling pathways in ofspring. Methods. Female Wistar rats were randomized into 3 groups: (1) control (CONT): fed a control diet preconceptionally and during pregnancy and lactation; (2) maternal high fat (MHF): fed an HF diet throughout their life and during pregnancy and lactation; (3) pregnancy and lactation HF (PLHF): fed a control diet throughout life until mating, then HF diet during pregnancy and lactation. Male ofspring were fed the control diet postweaning. Plasma and pancreatic tissue were collected, and mRNA concentrations of key factors regulating adipoinsular axis signaling were determined. Results. MHF and PLHF ofspring exhibited increased adiposity and were hyperinsulinemic and hyperleptinemic compared to CONT. Despite a similar anthropometric phenotype, MHF and PLHF ofspring exhibited distinctly diferent expression for key pancreatic genes, dependent upon maternal preconceptional nutritional background. Conclusions. hese data suggest that despite using diferential signaling pathways, obesity in ofspring may be an adaptive outcome of early life exposure to HF during critical developmental windows. 1. Introduction Early life events contribute substantially to the likelihood of an individual becoming obese, although underlying mech- anisms are not well understood. Obesity in women of reproductive age (15 to 44 years) is increasing rapidly, and up to 50% of women in this age range in the USA are now either overweight or obese [1]. his has translated to an exponential increase in the prevalence of obesity during pregnancy with up to 20% of women entering pregnancy with a BMI which would deine them as obese [2]. Obesity in pregnancy increases the risks for complications of pregnancy including miscarriage, hypertension, and gestational diabetes [3–5]. Furthermore, it is now well established that maternal obesity leads to an increased risk of obesity and metabolic and cardiovascular disorders in ofspring [6–9]. In view of the rising prevalence of obesity in pregnancy and its association with adverse maternal and ofspring outcomes, there is a great deal of interest in understanding the mechanistic pathways that link maternal obesity and excess maternal nutrition to increased risk of disease in childhood and beyond [10–13]. Clinical and experimental studies have consistently shown that maternal obesity predicts obesity, associated metabolic comorbidities, and reproductive disorders in adult ofspring [2, 14–16], oten underpinned by a proinlammatory status. However, there is a need to understand the relative contributions and interactions between maternal prepreg- nancy obesity and a gestational obesogenic environment