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Dipali Goyal, Sean W Limesand and Ravi Goyal

.6809.1019 1954451 Hanson MA Gluckman PD 2008 Developmental origins of health and disease: new insights . Basic and Clinical Pharmacology and Toxicology 102 90 – 93 . ( ) 10.1111/j.1742-7843.2007.00186.x

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Folami Y Ideraabdullah, Anthony M Belenchia, Cheryl S Rosenfeld, Seth W Kullman, Megan Knuth, Debabrata Mahapatra, Michael Bereman, Edward D Levin and Catherine A Peterson

disease in later life, also termed developmental origins of health and disease (DOHaD) ( Brannon 2012 , Reichetzeder et al. 2014 , Chango & Pogribny 2015 ). Animal models have been designed to elucidate the DOHaD effects of this secosteroid hormone

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Tessa J Roseboom

deciding the time of onset and severity of type 2 diabetes. Evidence for the developmental origins of health and disease Studies across the world have consistently shown that babies who were small at birth have increased rates of chronic

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Takeshi Iwasa, Toshiya Matsuzaki, Kiyohito Yano, Yiliyasi Mayila, Rie Yanagihara, Yuri Yamamoto, Akira Kuwahara and Minoru Irahara

in adulthood, especially under high nutrient conditions ( Godfrey & Barker 2000 , Breier et al. 2001 ). This concept, referred to as developmental origins of health and disease (DOHaD), may have important medical, biophysical and socioeconomic

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Valentina Pampanini, Daniela Germani, Antonella Puglianiello, Jan-Bernd Stukenborg, Ahmed Reda, Iuliia Savchuk, Kristín Rós Kjartansdóttir, Stefano Cianfarani and Olle Söder

in adulthood . Reproduction 125 769 – 784 . ( doi:10.1530/rep.0.1250769 ) Silveira PP Portella AK Goldani MZ Barbieri MA 2007 Developmental origins of health and disease (DOHaD) . Jornal de Pediatria 83 494 – 504 . ( doi

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Patrycja A Jazwiec and Deborah M Sloboda

disease risk. The hypothesis that the early life environment influences later life disease susceptibility is now recognized as the Developmental Origins of Health and Disease (DOHaD). Programming reproduction It is now known that non

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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

circulating hormones ( Björntorp & Sjöström 1971 ). Obesity is the result of a complex interaction between genetic and environmental factors ( Bouchard 2009 ). According to the Developmental Origin of Health and Disease (DOHaD) concept also called

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Christophe Breton

and high birth weight predisposing for the onset of later obesity. Originally called the Barker hypothesis or foetal programming, these observations have led to the Developmental Origin of Health and Disease (DOHaD) hypothesis ( Fernandez

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Chia-Lei Lin, Lyda Williams, Yoshinori Seki, Harpreet Kaur, Kirsten Hartil, Ariana Fiallo, A Scott Glenn, Ellen B Katz, Maureen J Charron and Patricia M Vuguin

Intrauterine (IU) malnutrition could alter pancreatic development. In this study, we describe the effects of high-fat diet (HFD) during pregnancy on fetal growth and pancreatic morphology in an ‘at risk’ animal model of metabolic disease, the glucose transporter 4 (GLUT4) heterozygous mouse (G4+/−). WT female mice mated with G4+/− males were fed HFD or control diet (CD) for 2 weeks before mating and throughout pregnancy. At embryonic day 18.5, fetuses were killed and pancreata isolated for analysis of morphology and expression of genes involved in insulin (INS) cell development, proliferation, apoptosis, glucose transport and function. Compared with WT CD, WT HFD fetal pancreata had a 2.4-fold increase in the number of glucagon (GLU) cells (P=0.023). HFD also increased GLU cell size by 18% in WT pancreata compared with WT CD. Compared with WT CD, G4+/− CD had an increased number of INS cells and decreased INS and GLU cell size. Compared with G4+/− CD, G4+/− HFD fetuses had increased pancreatic gene expression of Igf2, a mitogen and inhibitor of apoptosis. The expression of genes involved in proliferation, apoptosis, glucose transport, and INS secretion was not altered in WT HFD compared with G4+/− HFD pancreata. In contrast to WT HFD pancreata, HFD exposure did not alter pancreatic islet morphology in fetuses with GLUT4 haploinsufficiency; this may be mediated in part by increased Igf2 expression. Thus, interactions between IU diet and fetal genetics may play a critical role in the developmental origins of health and disease.

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Kok Lim Kua, Shanming Hu, Chunlin Wang, Jianrong Yao, Diana Dang, Alexander B Sawatzke, Jeffrey L Segar, Kai Wang and Andrew W Norris

Offspring exposed in utero to maternal diabetes exhibit long-lasting insulin resistance, though the initiating mechanisms have received minimal experimental attention. Herein, we show that rat fetuses develop insulin resistance after only 2-day continuous exposure to isolated hyperglycemia starting on gestational day 18. Hyperglycemia-induced reductions in insulin-induced AKT phosphorylation localized primarily to fetal skeletal muscle. The skeletal muscle of hyperglycemia-exposed fetuses also exhibited impaired in vivo glucose uptake. To address longer term impacts of this short hyperglycemic exposure, neonates were cross-fostered and examined at 21 days postnatal age. Offspring formerly exposed to 2 days late gestation hyperglycemia exhibited mild glucose intolerance with insulin signaling defects localized only to skeletal muscle. Fetal hyperglycemic exposure has downstream consequences which include hyperinsulinemia and relative uteroplacental insufficiency. To determine whether these accounted for induction of insulin resistance, we examined fetuses exposed to late gestational isolated hyperinsulinemia or uterine artery ligation. Importantly, 2 days of fetal hyperinsulinemia did not impair insulin signaling in murine fetal tissues and 21-day-old offspring exposed to fetal hyperinsulinemia had normal glucose tolerance. Similarly, fetal exposure to 2-day uteroplacental insufficiency did not perturb insulin-stimulated AKT phosphorylation in fetal rats. We conclude that fetal exposure to hyperglycemia acutely produces insulin resistance. As hyperinsulinemia and placental insufficiency have no such impact, this occurs likely via direct tissue effects of hyperglycemia. Furthermore, these findings show that skeletal muscle is uniquely susceptible to immediate and persistent insulin resistance induced by hyperglycemia.