Fetal growth restriction: adaptations and consequences

McMillen, I. C.; Mb, Adams; Ross, JT; Coulter, Catherine; Simonetta, Giuseppe; Owens, Julie A.; Robinson, J. S.; Edwards, LJ

doi:10.1530/rep.0.1220195

Cited by 234 publications

(174 citation statements)

References 21 publications

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“…Several different experimental approaches have been used to produce placental insufficiency with resultant fetal growth restriction in small and large animal models, including surgical removal of the majority of endometrial caruncles from the uterus of the non-pregnant ewe prior to mating [22,23]. This procedure restricts the number of placentomes that are formed from the beginning of pregnancy, thereby limiting placental growth and function.…”

Section: The Placental Origins Of Accelerated Postnatal Growthmentioning

confidence: 99%

“…This procedure restricts the number of placentomes that are formed from the beginning of pregnancy, thereby limiting placental growth and function. The placental delivery of oxygen and glucose to the fetus is restricted, and produces fetal hypoxaemia, hypoglycaemia and hypoinsulinaemia in late gestation and asymmetrical fetal growth [22][23][24][25]. There is evidence that there is a redistribution of cardiac output as the growth of the fetal brain, adrenal and heart are relatively spared, whereas fetal muscle, gut and liver mass are decreased [22][23][24][25].…”

Section: The Placental Origins Of Accelerated Postnatal Growthmentioning

confidence: 99%

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Fetal growth restriction, catch-up growth and the early origins of insulin resistance and visceral obesity

et al. 2009

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There is an association between growing slowly before birth, accelerated growth in early postnatal life and the emergence of insulin resistance, visceral obesity and glucose intolerance in adult life. In this review we consider the pathway through which intrauterine growth restriction (IUGR) leads to the initial increase in insulin sensitivity and to catch-up growth. We also discuss the importance of the early insulin environment in determining later visceral adiposity and the intrahepatic mechanisms that may result in the emergence of glucose intolerance in a subset of IUGR infants. We present evidence that a key fetal adaptation to poor fetal nutrition is an upregulation of the abundance of the insulin receptor in the absence of an upregulation of insulin signalling in fetal skeletal muscle. After birth, however, there is an upregulation in the abundance of the insulin receptor and the insulin signalling pathway in the IUGR offspring. Thus, the origins of the accelerated postnatal growth rate experienced by IUGR infants lie in the fetal adaptations to a poor nutrient supply. We also discuss how the intracellular availability of free fatty acids and glucose within the visceral adipocyte and hepatocyte in fetal and neonatal life are critical in determining the subsequent metabolic phenotype of the IUGR offspring. It is clear that a better understanding of the relative contributions of the fetal and neonatal nutrient environment to the regulation of key insulin signalling pathways in muscle, visceral adipose tissue and the liver is required to support the development of evidence-based intervention strategies and better outcomes for the IUGR infant.

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Section: The Placental Origins Of Accelerated Postnatal Growthmentioning

confidence: 99%

Section: The Placental Origins Of Accelerated Postnatal Growthmentioning

confidence: 99%

Fetal growth restriction, catch-up growth and the early origins of insulin resistance and visceral obesity

et al. 2009

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“…There is now overwhelming evidence that intrauterine growth retardation (IUGR) in humans is a strong determinant for several pathologies, including insulin resistance, type 2 diabetes, hypertension, and ischemic heart disease in later life [1]. These associations are independent of adult life-style.…”

Section: Introductionmentioning

confidence: 99%

Altered Control of the Hypothalamo-Pituitary-Adrenal Axis in Adult Male Rats Exposed Perinatally to Food Deprivation and/or Dehydration

et al. 2002

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Dehydration, a classic homeostatic stressor in rats, leads to a series of well characterized endocrine responses including stimulation of the hypothalamo-pituitary-adrenal (HPA) axis. In this study, the hypothesis to be tested was that a 50% maternal food restriction (FR50) in late gestation and lactation may have long-term repercussions on HPA axis responsiveness to dehydration in offspring. For this purpose, we studied HPA axis activity in 4-month-old control (C) and perinatally malnourished male rats after a 72-hour water deprivation period. Furthermore, we investigated the long-lasting effects of perinatal maternal malnutrition on the basal activity of the HPA axis. Under basal conditions, rats exposed to perinatal malnutrition showed reduced body weight, enhanced mineralocorticoid receptor (MR) mRNA levels in CA2 and CA3 hippocampal areas, but decreased glucocorticoid receptor (GR) mRNA levels in CA1, CA3 and dentate gyrus (DG) areas. In contrast, the levels of corticotropin-releasing hormone (CRH) and vasopressin (VP) mRNAs in the hypothalamic paraventricular nucleus (PVN) as well as of VP mRNA in the supraoptic nucleus (SON) were unaffected by maternal undernutrition. Expression of proopiomelanocortin (POMC) in the adenohypophysis was significantly enhanced, whereas prohormone convertase-1 (PC1) was not affected. Perinatal malnutrition reduced absolute adrenal weight but did not affect circulating levels of adrenocorticotropin (ACTH), corticosterone and free corticosterone as well as corticosteroid-binding globulin (CBG) binding capacity. Seventy-two hours of dehydration induced a decrease in body weight and CRH mRNA levels in PVN of controls as well as of FR50 rats, but also led to a rise in plasma corticosterone and free corticosterone without changing CBG binding capacity. Dehydration also induced an increase in adenopituitary POMC (C) and PC1 (FR50), PVN and SON VP (C) and GR in CA1 hippocampal area (FR50) mRNA levels and plasma ACTH (C), but a decrease in MR in DG (C) and GR in CA3 and DG (C) mRNA levels. We conclude that maternal food restriction during the perinatal period affects (1) the adult basal activity of the HPA axis with mainly opposite effects on hippocampal MR and GR gene expression and an increase in adenopituitary POMC gene expression, and (2) the responsiveness to water deprivation in adults. In the latter case, the rise in plasma ACTH levels, adenopituitary POMC gene expression, hypothalamic VP gene expression, and the decrease in hippocampal MR gene expression in DG and GR gene expression in CA3 and DG observed in controls are lacking in FR50 rats. In contrast, drastic adenopituitary PC1 gene expression occurred in FR50 rats but not in control animals.

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“…However, the same adjustments may become maladaptive when the foetus is born into conditions of abundant food supply. For example, intrauterine growth restriction in developed countries has been linked to a range of long-term health consequences, including increased susceptibility to develop cardiovascular disease, systolic hypertension, obesity, insulin resistance and diabetes type 2 [22,23]. The early-life environment is thus an important determinant of later-life health status.…”

Section: Early-life Programming Of Health and Diseasementioning

confidence: 99%

Factors in Early-Life Programming of Reproductive Fitness

2015

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Fertility rates have been declining worldwide, with a growing number of young women suffering from infertility. Infectious and inflammatory diseases are important causes of infertility, and recent evidence points to the critical role of the early-life microbial environment in developmental programming of adult reproductive fitness. Our laboratory and others have demonstrated that acute exposure to an immunological challenge early in life has a profound and prolonged impact on male and female reproductive development. This review presents evidence that perinatal exposure to immunological challenge by a bacterial endotoxin, lipopolysaccharide, acts at all levels of the hypothalamic-pituitary-gonadal axis, resulting in long-lasting changes in reproductive function, suggesting that disposition to infertility may begin early in life.

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Fetal growth restriction: adaptations and consequences

Abstract: Block BS, Schlafer DH, Wentworth RA, Kreitzer LA and Nathanielsz PW (1990) MA (1993)

Cited by 234 publications

References 21 publications

Fetal growth restriction, catch-up growth and the early origins of insulin resistance and visceral obesity

Fetal growth restriction, catch-up growth and the early origins of insulin resistance and visceral obesity

Altered Control of the Hypothalamo-Pituitary-Adrenal Axis in Adult Male Rats Exposed Perinatally to Food Deprivation and/or Dehydration

Factors in Early-Life Programming of Reproductive Fitness

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