%0 Journal Article
%T 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?
%A Graham J. Howie
%A Deborah M. Sloboda
%A Clare M. Reynolds
%A Mark H. Vickers
%J Journal of Nutrition and Metabolism
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/517384
%X Objective. Offspring 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 differential regulation of pancreatic adipoinsular and inflammatory signaling pathways in offspring. 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 offspring 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 offspring exhibited increased adiposity and were hyperinsulinemic and hyperleptinemic compared to CONT. Despite a similar anthropometric phenotype, MHF and PLHF offspring exhibited distinctly different expression for key pancreatic genes, dependent upon maternal preconceptional nutritional background. Conclusions. These data suggest that despite using differential signaling pathways, obesity in offspring 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 mechanisms 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]. This 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 define them as obese [2]. Obesity in pregnancy increases the risks for complications of pregnancy including miscarriage, hypertension, and gestational diabetes [3¨C5]. Furthermore, it is now well established that maternal obesity leads to an increased risk of obesity and metabolic and cardiovascular disorders in offspring [6¨C9]. In view of the rising prevalence of obesity in pregnancy and its association with adverse maternal and offspring outcomes, there is a great deal of interest in understanding the mechanistic pathways that link maternal obesity and excess maternal nutrition to increased
%U http://www.hindawi.com/journals/jnme/2013/517384/