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Caiping Mao, Rong Liu, Le Bo, Ningjing Chen, Shigang Li, Shuixiu Xia, Jie Chen, Dawei Li, Lubo Zhang and Zhice Xu

and fetal growth, inducing sodium-dependent hypertension in rats ( Barron et al . 2001 , Sanders et al . 2005 ). Recent studies in our laboratory showed alterations in body fluid homeostasis and blood pressure in the offspring exposed to maternal

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Yuhui Liu, Le Zhang, Jing Li, Zhongyan Shan and Weiping Teng

et al . 2005 ). It has been shown that the cognitive performance of offspring is severely affected by moderate-to-severe iodine deficiency in pregnant women. However, studies investigating the impacts of marginal iodine deficiency in pregnant women on

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Adina Maniu, Graham W Aberdeen, Terrie J Lynch, Jerry L Nadler, Soon O K Kim, Michael J Quon, Gerald J Pepe and Eugene D Albrecht

and the mechanisms integral to fetal development that prepare the offspring for controlling insulin secretion and action and glucose homeostasis after birth. We have shown that the baboon provides a superb nonhuman primate translational model for the

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Elena Zambrano, Tonantzin Sosa-Larios, Lizbeth Calzada, Carlos A Ibáñez, Carmen A Mendoza-Rodríguez, Angélica Morales and Sumiko Morimoto

worldwide and is an important risk factor contributing to type 2 diabetes in offspring ( Wang & Lobstein 2006 , Samuelsson et al . 2008 , Gonzalez et al . 2013 , Latouche et al . 2014 ). Type 2 diabetes is polygenic and may involve polymorphisms in

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Simon Lecoutre, Barbara Deracinois, Christine Laborie, Delphine Eberlé, Céline Guinez, Polina E Panchenko, Jean Lesage, Didier Vieau, Claudine Junien, Anne Gabory and Christophe Breton

sensitize offspring to obesity ( Leddy et al. 2008 ). Thus, WAT may represent a prime target of metabolic programming induced by maternal obesity. Perturbations to the perinatal nutrient supply may affect adipocyte development, leading to persistent

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Jin-Ran Chen, Oxana P Lazarenko, Haijun Zhao, Alexander W Alund and Kartik Shankar

( Vrtačnik et al . 2014 ). These mechanisms of epigenetics are important in regulating differentiation of different types of cells during both prenatal and postnatal development. Maternal nutrition appears to influence epigenetic alterations in the offspring

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Bo He, Yinxian Wen, Shuwei Hu, Guihua Wang, Wen Hu, Jacques Magdalou, Liaobin Chen and Hui Wang

have demonstrated that PCE can lead to fetal overexposure to maternal glucocorticoids and hypothalamic-pituitary-adrenal (HPA) axis-associated neuroendocrine metabolic programming alterations, resulting in the increased susceptibility of adult offspring

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J S M Cuffe, E L Turton, L K Akison, H Bielefeldt-Ohmann and K M Moritz

Introduction Maternal stress can impair foetal growth and program offspring susceptibility to adult onset disease ( Cottrell & Seckl 2009 ). Stress-induced impairment of foetal development is mediated by elevated maternal glucocorticoids

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Christophe Breton

perinatal nutritional manipulation on offspring hypothalamus–adipose axis. It mainly focuses on studies in rodents. We then summarise the possible developmental programming mechanisms underlying long-lasting perturbation of this axis throughout life

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Anthony M Belenchia, Sarah A Johnson, Mark R Ellersieck, Cheryl S Rosenfeld and Catherine A Peterson

VDD ( Reichetzeder et al . 2014 , Maia-Ceciliano et al . 2016 ). Yet, data are lacking on the specific effects of maternal VDD on offspring propensity for excess adiposity and/or associated metabolic complications. Aims of this study presented