Search Results

You are looking at 1 - 10 of 24 items for :

  • "developmental origins of health and disease" x
Clear All
Restricted access

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

Open access

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

Free access

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

Free access

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

Restricted access

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.

Free access

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.

Free access

Frank H Bloomfield

Disease. Journal of the Developmental Origins of Health and Disease 6 S138 – S139 . ( https://doi.org/10.1017/S2040174415007801 ) 10.1017/S2040174415007801) Bansal A Bloomfield FH Connor KL Dragunow M Thorstensen EB Oliver MH Sloboda

Restricted access

Sonnet S Jonker, Daniel Kamna, Dan LoTurco, Jenai Kailey and Laura D Brown

, Brown & Hay 2016 ). These fetal adaptations have life-long health implications, a phenomenon known as the Developmental Origins of Health and Disease first articulated by Barker and colleagues ( de Boo & Harding 2006 , Fernandez-Twinn & Ozanne 2010

Free access

Melanie Tran, Linda A Gallo, Andrew J Jefferies, Karen M Moritz and Mary E Wlodek

, Styrud et al . 2005 ). This association has been conceptualized by the developmental origins of health and disease hypothesis, whereby alterations in the fetal and postnatal environments influence the development of key metabolic organs involved, leading

Free access

Trassanee Chatmethakul and Robert D Roghair

pressure dysregulation in adult chickens . Journal of Developmental Origins of Health and Disease 4 69 – 76 . ( https://doi.org/10.1017/S204017441200058X ) 10.1017/S204017441200058X 25080183 Hinchliffe SA Sargent PH Howard CV Chan YF van Velzen D