Fetal programming of human disease

Barker, D. J. P.; Sultan, Hawra’a

doi:10.1017/cbo9780511570230.011

Cited by 15 publications

(10 citation statements)

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“…A sustained hypoxia forces an adaptational shift to less oxygen demand (Bocking et al, 1988;Bocking, 1993), reduced DNA synthesis (Hooper et al, 1991) and growth, with a gradual return towards normal concentrations of blood gasses and endocrine status (Challis et al, 1989), though with a residual deviation that may have a long-lasting effect on the fetal and newborn life. There is an increasing awareness that even subtle differences in the development of autocrine, paracrine, endocrine and metabolic functions induced by nutritional or circulatory variations during pregnancy could have lasting effects with increased risks of cardiovascular and endocrine diseases in adult life (Barker and Sultan, 1995).…”

Section: Circulatory Regulationmentioning

confidence: 99%

The fetal circulation

2004

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Accumulating data on the human fetal circulation shows the similarity to the experimental animal physiology, but with important differences. The human fetus seems to circulate less blood through the placenta, shunt less through the ductus venosus and foramen ovale, but direct more blood through the lungs than the fetal sheep. However, there are substantial individual variations and the pattern changes with gestational age. The normalised umbilical blood flow decreases with gestational age, and, at 28 to 32 weeks, a new level of development seems to be reached. At this stage, the shunting through the ductus venosus and the foramen ovale reaches a minimum, and the flow through the lungs a maximum. The ductus venosus and foramen ovale are functionally closely related and represent an important distributional unit for the venous return. The left portal branch represents a venous watershed, and, similarly, the isthmus aorta an arterial watershed. Thus, the fetal central circulation is a very flexible and adaptive circulatory system. The responses to increased afterload, hypoxaemia and acidaemia in the human fetus are equivalent to those found in animal studies: increased ductus venosus and foramen ovale shunting, increased impedance in the lungs, reduced impedance in the brain, increasingly reversed flow in the aortic isthmus and a more prominent coronary blood flow.

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Section: Circulatory Regulationmentioning

confidence: 99%

The fetal circulation

2004

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“…Special features of antenatal programming include: critical periods of vulnerability, failure or unsatisfactory completion of specific developmental milestones, association with functional defects, the permanent nature of such sequelae, and so forth (Barker, 1989a; 1989b; 1992; 1994; 1995a; 1995b; 1998; 2004; Barker et al , 1995; Nijland et al , 2008). The concept of the developmental origins of adult health and disease, first articulated by David J.P. Barker in the mid-1980s, “... suggested that poor nutrition in early life increases susceptibility to the effects of an affluent diet” (Barker & Osmond, 1986a).…”

Section: Introductionmentioning

confidence: 99%

“…These include studies correlating adult mortality from acute myocardial infarction with high infant mortality rates in a given population, follow-up studies correlating adult hypertension, coronary artery disease, and type II diabetes with low birth weight, the relation of increased mortality from coronary artery disease to low weight at 1 yr of age, and the relation of both newborn ponderal index [weight (g) x 10 2 /crown-heel length (cm) 2 ] and placental-to-fetal weight ratio to hypertension in the adult (see Barker, 2003, and Barker et al , 1995 for review). These associations are independent of adult life style risk factors (Barker et al , 1993).…”

Section: Introductionmentioning

confidence: 99%

Gene expression in the placenta: maternal stress and epigenetic responses

Gheorghe

Goyal

Mittal³

et al. 2010

Int. J. Dev. Biol.

133

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Successful placental development is crucial for optimal growth, development, maturation and survival of the embryo/fetus into adulthood. Numerous epidemiologic and experimental studies have demonstrated the profound influence of intrauterine environment on life, and the diseases to which one is subject as an adult. For the most part, these invidious influences, whether maternal hypoxia, protein or caloric deficiency or excess, and others, represent types of maternal stress. In the present review, we examine certain aspects of gene expression in the placenta as a consequence of maternal stressors. To examine these issues in a controlled manner, and in a species in which the genome has been sequenced, most of these reported studies have been performed in the mouse. Although each individual maternal stress is characterized by up-or down-regulation of specific genes in the placenta, functional analysis reveals some patterns of gene expression common to the several forms of stress. Of critical importance, these genes include those involved in DNA methylation and histone modification, cell cycle regulation, and related global pathways of great relevance to epigenesis and the developmental origins of adult health and disease.

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“…A series of worldwide epidemiological studies in the past decade have highlighted the potential importance of fetal adaptations to a poor intra‐uterine environment for longer term health outcomes 1–4 . These studies have demonstrated that there are significant relationships between birthweight or birth phenotype and the relative risk of onset of ischaemic heart disease, hypertension and non‐insulin‐dependent diabetes.…”

Section: Introductionmentioning

confidence: 99%

Prenatal Undernutrition, Glucocorticoids And The Programming Of Adult Hypertension

Edwards

Coulter

Symonds

et al. 2001

Clin Exp Pharma Physio

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1. A range of epidemiological studies has shown that poor intra-uterine growth is associated with an increased prevalence of cardiovascular disease, non-insulin-dependent diabetes mellitus and the Metabolic syndrome in adult life. 2. Because these associations are independent of adult lifestyle or current size, it has been postulated that a reduced intra- uterine nutrient supply perturbs fetal growth and, concomitantly, alters or programmes the structure and function of developing systems. 3. A reduced fetal nutrient supply may be a consequence of poor placental function or inadequate maternal nutrient intake. 4. It has been proposed that one outcome of either a suboptimal placental or maternal nutrient supply is exposure of the fetus to excess glucocorticoids, which act to restrict fetal growth and to programme permanent changes in the cardiovascular, endocrine and metabolic systems. 5. While a range of studies in the rat has investigated the impact of maternal undernutrition on arterial blood pressure in the offspring, there have been relatively few studies in species, such as the sheep, in which the responses of the cardiovascular and neuroendocrine systems to intra-uterine undernutrition can be measured before birth. 6. The present review summarizes recent evidence that poor placental function or inadequate maternal nutrition each results in an increased exposure of fetal sheep tissues to glucocorticoids and, in specific, changes in the regulation of fetal arterial blood pressure. 7. These studies are important in determining how the timing, type and duration of fetal nutrient restriction are each important in determining the nature of the fetal neuroendocrine and cardiovascular adaptive responses and their pathophysiological sequelae in later life.

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Fetal programming of human disease

Cited by 15 publications

References 0 publications

The fetal circulation

The fetal circulation

Gene expression in the placenta: maternal stress and epigenetic responses

Prenatal Undernutrition, Glucocorticoids And The Programming Of Adult Hypertension

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