Increased systolic blood pressure in rats induced by a maternal low-protein diet is reversed by dietary supplementation with glycine

Jackson, Alan A.; Dunn, Rebecca L.; Marchand, Michael C.; Langley‐Evans, Simon C.

doi:10.1042/cs1030633

Cited by 213 publications

(143 citation statements)

References 32 publications

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“…This may promote disturbances of the methionine-homocysteine cycle that impact upon the provision of methyl donors for methylation of DNA. This view is supported by evidence from a number of studies in which the MLP diet is supplemented with folic acid [24], or with glycine [12]. These generally show that the effects of low-protein feeding can be reversed.…”

Section: Dna Methylation and Epigenetic Programmingsupporting

confidence: 67%

Metabolic programming in pregnancy: studies in animal models

Langley‐Evans

2007

Genes Nutr

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The developmental origins of adult disease hypothesisEpidemiological studies of many large populations indicate that non-communicable diseases in adulthood are related to factors in fetal life or during infancy [1]. Low birthweight or disproportion at birth are associated with increased risk of cardiovascular disease and type-II diabetes. These associations have been explained in terms of developmental programming, which is the process through which insults or stimuli during early life exert permanent effects upon organ development, physiology and metabolism [18]. Variation in the nutrient supply during fetal has been proposed as the major programming stimulus that determines risk of disease in adulthood.Studies of human cohorts have mainly required the use of retrospective cohorts and this has raised serious issues regarding control for confounding factors, selection bias and measurement bias [11]. Moreover, within relatively well-nourished populations variation in maternal nutrient intakes are noted to have little impact upon patterns of fetal growth or birthweight [17], which has led some observers to question the plausibility of the developmental origins of adult disease hypothesis. Experimental studies employing small animal species (e.g. rat, mouse or guinea pig) or larger species (pig and sheep) have, however, clearly demonstrated the biological plausibility of nutritional programming [25]. A diverse range of nutritional manipulations in pregnancy have been shown to programme profound changes in tissue morphology, physiology and metabolism and often these changes occur independently of fetal growth retardation [25]. Animal models of cardiovascular programmingAlthough the approaches used to manipulate the maternal diet in order to test the developmental programming hypothesis have been varied, cardiovascular changes in the resultant offspring are a near universal outcome. Global nutrient restriction during pregnancy (controlled reductions of maternal nutrient intake) in rodents [36] and in sheep [9] produces small changes in blood pressure in the adult offspring, which often only manifest at maturity. Similar delays in the appearance of blood pressure changes are noted with the feeding of high-saturated fat diets [15] or iron deficient diets [8] to pregnant rats. In contrast the marked increase in blood pressure and variation in vascular reactivity to vasoconstrictors and relaxants that follows intrauterine protein restriction [7,16] tends to manifest very early in the postnatal period (Fig. 1).One of the major drawbacks of working with rodent species is the fact that these are generally resistant to the development of atherosclerosis. Thus, whilst nutritional programming of cardiovascular risk factors is demonstrable, the development of coronary heart disease is difficult to model in animals. Ongoing studies with transgenic lines which develop vascular lesions in response to high fat-high cholesterol diets, for example the apo E*3 Leiden strain [10], will yield important data in this area over the next fe...

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Section: Dna Methylation and Epigenetic Programmingsupporting

confidence: 67%

Metabolic programming in pregnancy: studies in animal models

Langley‐Evans

2007

Genes Nutr

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“…Arginine and arginine-family amino acids recently have been discovered to be abundant in ovine and porcine allantoic fluids, indicating their importance in fetal development (Lillycrop et al 2005). With regard to glycine, supplementation of a protein-restricted gestational diet with glycine reverses the increase in systolic blood pressure that occurs in the offspring of protein-restricted dams (Jackson et al 2002). Maternal protein restriction is known to negatively impact kidney function by reducing nephron number and result in hypertension in offspring (Langley-Evans et al 1999).…”

Section: Discussionmentioning

confidence: 99%

Dietary soya protein during pregnancy and lactation in rats with hereditary kidney disease attenuates disease progression in offspring

et al. 2007

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Dietary soya protein substitution for casein initiated at weaning slows disease progression in animal models of chronic renal disease. As there is increasing evidence that fetal programming can have a significant impact on kidney physiology and function in offspring, the objective of the current study was to determine whether exposure to soya protein in the diet earlier than weaning would have further benefits. Han:SPRD-cy (cy/þ ) breeder rats were fed a casein-based or soya protein-based diet 2 weeks prior to mating, throughout pregnancy and during lactation. Following this maternal period, 3-week-old pups were given either the same or the alternate diet for a 7-week weaning period. Dietary soya protein compared with casein in the maternal or weaning period both independently resulted in less renal inflammation (macrophage infiltration lower by 24 % (P¼ 0·0003) and 32 % (P, 0·0001), respectively). When soya protein was given in both feeding periods, the effect was additive. Soya protein substitution for casein resulted in less oxidative damage as indicated by 28 % lower oxidized-LDL staining (P¼ 0·013) when present in the maternal period, or in the weaning period (by 56 %, P,0·0001). Renal cell proliferation was reduced by 29-33 % (P,0·05) in rats given soya protein whether the exposure was during the maternal or weaning period. Soya protein compared with casein in the maternal period also resulted in 33 % (P¼ 0·0013) less proteinuria, indicating superior renal function. Dietary soya protein during pregnancy and lactation represents a potential preventative approach in treating for those with congenital kidney diseases.

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“…11 Supplementation of low protein diets with glycine or folate reverses the programming effect of those diets. 12,13 However such a mechanism may lack gene specificity, whereas other data argues that it is specific genes that are susceptible to this effect. 14 -17 Thus in this study we set out to test the hypothesis that alteration of DNA methylation of 1 or more RAS component genes might underlie the alteration of gene expression that culminated in the development of hypertension.…”

mentioning

confidence: 92%

Epigenetic Modification of the Renin-Angiotensin System in the Fetal Programming of Hypertension

Bogdarina

Welham

King

et al. 2007

Circulation Research

452

297

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Abstract-Hypertension is a major risk factor for cardiovascular and cerebrovascular disease. Lifelong environmental factors (eg, salt intake, obesity, alcohol) and genetic factors clearly contribute to the development of hypertension, but it has also been established that stress in utero may program the later development of the disease. This phenomenon, known as fetal programming can be modeled in a range of experimental animal models. In maternal low protein diet rat models of programming, administration of angiotensin converting enzyme inhibitors or angiotensin receptor antagonists in early life can prevent development of hypertension, thus implicating the renin-angiotensin system in this process. Here we show that in this model, expression of the AT 1b angiotensin receptor gene in the adrenal gland is upregulated by the first week of life resulting in increased receptor protein expression consistent with the increased adrenal angiotensin responsiveness observed by others. Furthermore, we show that the proximal promoter of the AT 1b gene in the adrenal is significantly undermethylated, and that in vitro, AT 1b gene expression is highly dependent on promoter methylation. These data suggest a link between fetal insults to epigenetic modification of genes and the resultant alteration of gene expression in adult life leading ultimately to the development of hypertension. It seems highly probable that similar influences may be involved in the development of human hypertension. (Circ Res. 2007;100:520-526.)

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Increased systolic blood pressure in rats induced by a maternal low-protein diet is reversed by dietary supplementation with glycine

Cited by 213 publications

References 32 publications

Metabolic programming in pregnancy: studies in animal models

Metabolic programming in pregnancy: studies in animal models

Dietary soya protein during pregnancy and lactation in rats with hereditary kidney disease attenuates disease progression in offspring

Epigenetic Modification of the Renin-Angiotensin System in the Fetal Programming of Hypertension

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