Manipulation of the Maternal Diet in Rat Pregnancy

Langley‐Evans, Simon C.; Bellinger, Leanne; Sculley, Dean V.; Langley-Evans, Alison J.; McMullen, Sarah

doi:10.1007/0-387-32632-4_8

Cited by 4 publications

(2 citation statements)

References 77 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is challenging to dissect out the effects of maternal obesity from the maternal diet in these experiments and both factors may have programming effects on specific features of metabolic and physiological function. Cafeteria feeding during lactation also influences offspring behaviours indicating that, in rats at least, the window for programming to occur is wide and that the mechanism may be independent of the intrauterine environment ( 39 , 64 ) .…”

Section: Animal Models Of Nutritional Programmingmentioning

confidence: 99%

Fetal programming of CVD and renal disease: animal models and mechanistic considerations

Langley‐Evans

2013

Proc. Nutr. Soc.

Self Cite

View full text Add to dashboard Cite

The developmental origins of health and disease hypothesis postulates that exposure to a less than optimal maternal environment during fetal development programmes physiological function, and determines risk of disease in adult life. Much evidence of such programming comes from retrospective epidemiological cohorts, which demonstrate associations between birth anthropometry and non-communicable diseases of adulthood. The assertion that variation in maternal nutrition drives these associations is supported by studies using animal models, which demonstrate that maternal under-or over-nutrition during pregnancy can programme offspring development. Typically, the offspring of animals that are undernourished in pregnancy exhibit a relatively narrow range of physiological phenotypes that includes higher blood pressure, glucose intolerance, renal insufficiency and increased adiposity. The observation that common phenotypes arise from very diverse maternal nutritional insults has led to the proposal that programming is driven by a small number of mechanistic processes. The remodelling of tissues during development as a consequence of maternal nutritional status being signalled by endocrine imbalance or key nutrients limiting processes in the fetus may lead to organs having irreversibly altered structures that may limit their function with ageing. It has been proposed that the maternal diet may impact upon epigenetic marks that determine gene expression in fetal tissues, and this may be an important mechanism connecting maternal nutrient intakes to long-term programming of offspring phenotype. The objective for this review is to provide an overview of the mechanistic basis of fetal programming, demonstrating the critical role of animal models as tools for the investigation of programming phenomena.

show abstract

Section: Animal Models Of Nutritional Programmingmentioning

confidence: 99%

Fetal programming of CVD and renal disease: animal models and mechanistic considerations

Langley‐Evans

2013

Proc. Nutr. Soc.

Self Cite

View full text Add to dashboard Cite

show abstract

“…Anything that disrupts this order is very likely to have consequences [42] , and in the simplest scenarios will result in organs that are smaller, due to a lower final cell number, or which are morphologically altered due to the presence of alternative cell types. This process has been termed tissue remodelling [43] . The tissue remodelling phenomenon has mostly been studied in kidney, by our group and others [44,45] .…”

Section: The Response To Intrauterine Insult: Mechanisms Of Programmimentioning

confidence: 99%

A common cause for a common phenotype: The gatekeeper hypothesis in fetal programming

et al. 2012

View full text Add to dashboard Cite

Sub-optimal nutrition during pregnancy has been shown to have long-term effects on the health of offspring in both humans and animals. The most common outcomes of such programming are hypertension, obesity, dyslipidaemia and insulin resistance. This spectrum of disorders, collectively known as metabolic syndrome, appears to be the consequence of nutritional insult during early development, irrespective of the nutritional stress experienced. For example, diets low in protein diet, high in fat, or deficient in iron are all associated with programming of cardiovascular and metabolic disorders when fed during rat pregnancy. In this paper, we hypothesise that the nutritional stresses act on genes or gene pathways common to all of the insults. We have termed these genes and/or gene pathways the “gatekeepers” and hence developed the “gatekeeper hypothesis”. In this paper, we examine the background to the hypothesis and postulate some possible mechanisms or pathways that may constitute programming gatekeepers.

show abstract

Early life fluoxetine treatment causes long-term lean phenotype in skeletal muscle of rats exposed to maternal lard-based high-fat diet

Visco

Manhães-de-Castro

Silva

et al. 2020

Biomedicine & Pharmacotherapy

View full text Add to dashboard Cite

Manipulation of the Maternal Diet in Rat Pregnancy

Cited by 4 publications

References 77 publications

Fetal programming of CVD and renal disease: animal models and mechanistic considerations

Fetal programming of CVD and renal disease: animal models and mechanistic considerations

A common cause for a common phenotype: The gatekeeper hypothesis in fetal programming

Early life fluoxetine treatment causes long-term lean phenotype in skeletal muscle of rats exposed to maternal lard-based high-fat diet

Contact Info

Product

Resources

About