Prenatal programming of renal salt wasting resets postnatal salt appetite, which drives food intake in the rat

Alwasel, Saleh; Barker, D. J. P.; Ashton, Nick

doi:10.1042/cs20110266

Cited by 25 publications

(10 citation statements)

References 37 publications

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“…Protein restriction throughout pregnancy in the rat results in offspring that are born small, develop high blood pressure (Woods et al 2001), impaired renal function (Alwasel et al 2012), glucose intolerance (Ozanne et al 1996), and impaired fertility (Zambrano et al 2005), suggesting that sustained nutritional deficits throughout pregnancy can elicit a wide variety of long-term abnormalities (Woods et al 2001(Woods et al , 2005. Short-term infusions of glucocorticoids during early-or midgestation culminate in hypertension in both sheep (Dodic et al 2002) and rat offspring respectively (Ortiz et al 2003, Singh et al 2007a.…”

Section: Perturbations Resulting In Developmental Programing: the Impmentioning

confidence: 99%

Adverse prenatal environment and kidney development: implications for programing of adult disease

Dorey¹,

Pantaleon²,

Weir³

2014

Reproduction

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The 'developmental origins of health and disease' hypothesis suggests that many adult-onset diseases can be attributed to altered growth and development during early life. Perturbations during gestation can be detrimental and lead to an increased risk of developing renal, cardiovascular, metabolic, and neurocognitive dysfunction in adulthood. The kidney has emerged as being especially vulnerable to insult at almost any stage of development resulting in a reduction in nephron endowment. In both humans and animal models, a reduction in nephron endowment is strongly associated with an increased risk of hypertension. The focus of this review is twofold: i) to determine the importance of specific periods during development on long-term programing and ii) to examine the effects of maternal perturbations on the developing kidney and how this may program adult-onset disease. Recent evidence has suggested that insults occurring around the time of conception also have the capacity to influence long-term health. Although epigenetic mechanisms are implicated in mediating these outcomes, it is unclear as to how these may impact on kidney development. This presents exciting new challenges and areas for research.Reproduction (2014) 147 R189-R198

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Section: Perturbations Resulting In Developmental Programing: the Impmentioning

confidence: 99%

Adverse prenatal environment and kidney development: implications for programing of adult disease

Dorey¹,

Pantaleon²,

Weir³

2014

Reproduction

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“…In addition, maternal low-protein diet increases the risk of salt-sensitive hypertension [57]. Observed salt sensitivity in an offspring may be due to increased expression of Na-K-2Cl (NKCC2) cotransporter in the thick ascending limb of the loop of Henle or decreased activity of the Na-K-ATPase in the inner medullary collecting duct [108, 109]. Administration of ouabain, a Na-K-ATPase ligand, to these rats abolished apoptosis and increased cell proliferation in the metanephric blastema [110, 111].…”

Section: Roles Of Lbw and Prematurity In Kidney Developmentmentioning

confidence: 99%

Developmental Programming of Hypertension and Kidney Disease

Chong

Yosypiv

2012

International Journal of Nephrology

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A growing body of evidence supports the concept that changes in the intrauterine milieu during “sensitive” periods of embryonic development or in infant diet after birth affect the developing individual, resulting in general health alterations later in life. This phenomenon is referred to as “developmental programming” or “developmental origins of health and disease.” The risk of developing late-onset diseases such as hypertension, chronic kidney disease (CKD), obesity or type 2 diabetes is increased in infants born prematurely at <37 weeks of gestation or in low birth weight (LBW) infants weighing <2,500 g at birth. Both genetic and environmental events contribute to the programming of subsequent risks of CKD and hypertension in premature or LBW individuals. A number of observations suggest that susceptibility to subsequent CKD and hypertension in premature or LBW infants is mediated, at least in part, by reduced nephron endowment. The major factors influencing in utero environment that are associated with a low final nephron number include uteroplacental insufficiency, maternal low-protein diet, hyperglycemia, vitamin A deficiency, exposure to or interruption of endogenous glucocorticoids, and ethanol exposure. This paper discusses the effect of premature birth, LBW, intrauterine milieu, and infant feeding on the development of hypertension and renal disease in later life as well as examines the role of the kidney in developmental programming of hypertension and CKD.

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“…Despite a large body of evidence that maternal undernutrition programmes various organs in the offspring [1]- [4], little is known about the effects of maternal food restriction on the reproductive system in female offspring over two generations [16] [17]. The aim of the present study was to investigate the effect of maternal food restriction during pregnancy on the structure and capacity of the uterus of female rats from the first and second generations.…”

Section: Introductionmentioning

confidence: 97%

Effect of Maternal Food Restriction on the Uterus of Female Rats from the First and Second Generation

Alwasel¹

2016

ARSci

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Postnatal life is affected by changes in fetal development due to adverse events. The present study examined the effect of maternal food restriction on uterine structure and capacity in female rats from the first and second generations (FR1 and FR2) before and after puberty. Pregnant rats were fed ad libitum (Control, C) or maintained under food-restriction conditions (50%FR) during pregnancy. After delivery, all groups were given free access to food. Females from the first generation (FR1) were divided into two subgroups for either uterine dissection or to produce the next generation (FR2). Similar to FR1, FR2 females were exposed to maternal food restriction following the same procedure. FR2 females were also assigned into two subgroups for either uterine dissection or for mating to examine pregnancy outcomes. Uteri from the C, FR1 and FR2 groups were dissected at 4 weeks of age (before puberty) or at 8 weeks of age (after puberty) to evaluate uterine weight and uterine horn length. Tissues were stained with eosin and haematoxylin for examination vialight microscopy. The results showed that food restriction did not affect uterine weight or uterine horn length in FR1 and FR2 females before puberty. However, there were effects of maternal food restriction on uterine weight and length at 8 weeks of age. Uterine weight and uterine horn length were significantly reduced in the FR1 and FR2 groups compared with the values of the controls. This was associated with changes in pregnancy outcomes. Litter size was not affected in the FR1 group; however, litter weight was significantly reduced, leading to an 18% reduction in pup weight at birth. Unlike with FR1 litters, the size of FR2 litters was significantly reduced, leading to a lower degree of pup body weight reduction at birth (only 7%). The gestational length was normal in FR1 females but was significantly decreased in FR2 females. No histopathological changes were observed. These results showed that the uterus was affected by maternal food restriction. It seemed that FR2 females had a different reproductive strategy: they tended to reduce litter size to maintain pup weight at birth. In conclusion, maternal food restriction affects the uteri of the first and second generation. Females from the FR1 and FR2 groups followed different reproductive strategies according to their previous experience with exposure to intrauterine food S. H. Alwasel 24 restriction.

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Prenatal programming of renal salt wasting resets postnatal salt appetite, which drives food intake in the rat

Cited by 25 publications

References 37 publications

Adverse prenatal environment and kidney development: implications for programing of adult disease

Adverse prenatal environment and kidney development: implications for programing of adult disease

Developmental Programming of Hypertension and Kidney Disease

Effect of Maternal Food Restriction on the Uterus of Female Rats from the First and Second Generation

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