scholarly journals Postnatal food restriction in the rat as a model for a low nephron endowment

2006 ◽  
Vol 291 (5) ◽  
pp. F1104-F1107 ◽  
Author(s):  
Michiel F. Schreuder ◽  
Jens R. Nyengaard ◽  
Floor Remmers ◽  
Joanna AE van Wijk ◽  
Henriette A. Delemarre-van de Waal
Keyword(s):  
Intrauterine Growth Restriction ◽  
Food Restriction ◽  
Kidney Development ◽  
Later Life ◽  
Growth Restriction ◽  
Suitable Model ◽  
Intrauterine Growth ◽  
Glomerular Volume ◽  
Nephron Endowment ◽  
Glomerular Number

A low nephron endowment may be associated with hypertension. Nephrogenesis is the process that leads to the formation of nephrons until week 36 of gestation in humans and may be inhibited by many factors like intrauterine growth restriction and premature birth. To study the consequences of a low glomerular number, animal models have been developed. We describe a model of postnatal food restriction in the rat in which litter size is increased to 20 pups, which leads to growth restriction. In the rat, active nephrogenesis continues until postnatal day 8, which coincides with the growth restriction in our model. Design-based stereological methods were used to estimate glomerular number and volume. Our results show an ∼25% lower glomerular number in rats after postnatal food restriction (30,800 glomeruli/kidney) compared with control rats (39,600 glomeruli/kidney, P < 0.001). Mean glomerular volume was increased by 35% in the growth-restricted rats ( P = 0.006). There was a significant negative correlation between glomerular volume and glomerular number ( r = −0.76, P < 0.001). We conclude that postnatal food restriction in the rat leads to a low nephron endowment with compensatory enlargement. It is therefore a suitable model to study the effect of intrauterine growth restriction or prematurity on kidney development and the consequences of a reduced glomerular number in later life.

Epigenetic mechanisms involved in intrauterine growth restriction and aberrant kidney development and function

2020 ◽  
pp. 1-11
Author(s):  
Thu N. A. Doan ◽  
Jessica F. Briffa ◽  
Aaron L. Phillips ◽  
Shalem Y. Leemaqz ◽  
Rachel A. Burton ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Intrauterine Growth Restriction ◽  
Kidney Development ◽  
Dna Methyltransferases ◽  
Growth Restriction ◽  
Epigenetic Mechanisms ◽  
Specific Expression ◽  
Maternal Line ◽  
Intrauterine Growth ◽  
Increased Risk

Abstract Intrauterine growth restriction (IUGR) due to uteroplacental insufficiency results in a placenta that is unable to provide adequate nutrients and oxygen to the fetus. These growth-restricted babies have an increased risk of hypertension and chronic kidney disease later in life. In rats, both male and female growth-restricted offspring have nephron deficits but only males develop kidney dysfunction and high blood pressure. In addition, there is transgenerational transmission of nephron deficits and hypertension risk. Therefore, epigenetic mechanisms may explain the sex-specific programming and multigenerational transmission of IUGR-related phenotypes. Expression of DNA methyltransferases (Dnmt1and Dnmt3a) and imprinted genes (Peg3, Snrpn, Kcnq1, and Cdkn1c) were investigated in kidney tissues of sham and IUGR rats in F1 (embryonic day 20 (E20) and postnatal day 1 (PN1)) and F2 (6 and 12 months of age, paternal and maternal lines) generations (n = 6–13/group). In comparison to sham offspring, F1 IUGR rats had a 19% decrease in Dnmt3a expression at E20 (P < 0.05), with decreased Cdkn1c (19%, P < 0.05) and increased Kcnq1 (1.6-fold, P < 0.01) at PN1. There was a sex-specific difference in Cdkn1c and Snrpn expression at E20, with 29% and 34% higher expression in IUGR males compared to females, respectively (P < 0.05). Peg3 sex-specific expression was lost in the F2 IUGR offspring, only in the maternal line. These findings suggest that epigenetic mechanisms may be altered in renal embryonic and/or fetal development in growth-restricted offspring, which could alter kidney function, predisposing these offspring to kidney disease later in life.

Searching the web: a survey on the quality of advice on postnatal sequelae of intrauterine growth restriction and the implication of developmental origins of health and disease

2017 ◽  
Vol 8 (5) ◽  
pp. 604-612 ◽  
Author(s):  
S. Perzel ◽  
H. Huebner ◽  
W. Rascher ◽  
C. Menendez-Castro ◽  
A. Hartner ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Later Life ◽  
Growth Restriction ◽  
Developmental Origins ◽  
Intrauterine Growth ◽  
Growing Body ◽  
Health Related ◽  
Health And Disease ◽  
The Individual

Intrauterine growth restriction (IUGR) and fetal growth restriction (FGR) are pregnancy complications associated with morbidity in later life. Despite a growing body of evidence from current research on developmental origins of health and disease (DOHaD), little information is currently provided to parents on long-term metabolic, cardiovascular and neurologic consequences. As parents strongly rely on internet-based health-related information, we examined the quality of information on IUGR/FGR sequelae and DOHaD in webpages used by laypersons. Simulating non-clinicians experience, we entered the terms ‘IUGR consequences’ and ‘FGR consequences’ into Google and Yahoo search engines. The quality of the top search-hits was analyzed with regard to the certification through the Health On the Net Foundation (HON), currentness of cited references, while reliability of information and DOHaD-related consequences were assessed via the DISCERN Plus score (DPS). Overall the citation status was not up-to-date and only a few websites were HON-certified. The results of our analysis showed a dichotomy between the growing body of evidence regarding IUGR/FGR-related sequelae and lack of current guidelines, leaving parents without clear directions. Furthermore, detailed information on the concept of DOHaD is not provided. These findings emphasize the responsibility of the individual physician for providing advice on IUGR/FGR-related sequelae, monitoring and follow-up.

scholarly journals Maternal food restriction‐induced intrauterine growth restriction in a rat model leads to sex‐specific adipogenic programming

2020 ◽  
Vol 34 (12) ◽  
pp. 16073-16085
Author(s):  
Sreevidya Sreekantha ◽  
Ying Wang ◽  
Reiko Sakurai ◽  
Jie Liu ◽  
Virender K. Rehan
Keyword(s):  
Rat Model ◽  
Intrauterine Growth Restriction ◽  
Food Restriction ◽  
Growth Restriction ◽  
Intrauterine Growth

Intrauterine growth restriction promotes vascular remodelling following carotid artery ligation in rats

2012 ◽  
Vol 123 (7) ◽  
pp. 437-444 ◽  
Author(s):  
Carlos Menendez-Castro ◽  
Nada Cordasic ◽  
Matthias Schmid ◽  
Fabian Fahlbusch ◽  
Wolfgang Rascher ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Intrauterine Growth Restriction ◽  
Later Life ◽  
Epidemiological Studies ◽  
Growth Restriction ◽  
Vascular Remodelling ◽  
Artery Ligation ◽  
Intrauterine Growth ◽  
Carotid Artery Ligation ◽  
Increased Risk

Epidemiological studies revealed an association between IUGR (intrauterine growth restriction) and an increased risk of developing CVDs (cardiovascular diseases), such as atherosclerosis or hypertension, in later life. Whether or not IUGR contributes to the development of atherosclerotic lesions, however, is unclear. We tested the hypothesis that IUGR aggravates experimentally induced vascular remodelling. IUGR was induced in rats by maternal protein restriction during pregnancy (8% protein diet). To detect possible differences in the development of vascular injury, a model of carotid artery ligation to induce vascular remodelling was applied in 8-week-old intrauterine-growth-restricted and control rat offspring. Histological and immunohistochemical analyses were performed in the ligated and non-ligated carotid arteries 8 weeks after ligation. IUGR alone neither caused overt histological changes nor significant dedifferentiation of VSMCs (vascular smooth muscle cells). After carotid artery ligation, however, neointima formation, media thickness and media/lumen ratio were significantly increased in rats after IUGR compared with controls. Moreover, dedifferentiation of VSMCs and collagen deposition in the media were more prominent in ligated carotids from rats after IUGR compared with ligated carotids from control rats. We conclude that IUGR aggravates atherosclerotic vascular remodelling induced by a second injury later in life.

scholarly journals Intrauterine growth restriction and adult disease: the role of adipocytokines

2009 ◽  
Vol 160 (3) ◽  
pp. 337-347 ◽  
Author(s):  
Despina D Briana ◽  
Ariadne Malamitsi-Puchner
Keyword(s):  
Adipose Tissue ◽  
Chronic Diseases ◽  
Intrauterine Growth Restriction ◽  
Subsequent Development ◽  
Later Life ◽  
Growth Restriction ◽  
Growth Potential ◽  
Intrauterine Growth ◽  
Thrifty Phenotype

Intrauterine growth restriction (IUGR) is the failure of the fetus to achieve his/her intrinsic growth potential, due to anatomical and/or functional disorders and diseases in the feto–placental–maternal unit. IUGR results in significant perinatal and long-term complications, including the development of insulin resistance/metabolic syndrome in adulthood.The thrifty phenotype hypothesis holds that intrauterine malnutrition leads to an adaptive response that alters the fetal metabolic and hormonal milieu designed for intrauterine survival. This fetal programming predisposes to an increased susceptibility for chronic diseases. Although the mechanisms controlling intrauterine growth are poorly understood, adipose tissue may play an important role in linking poor fetal growth to the subsequent development of adult diseases. Adipose tissue secretes a number of hormones, called adipocytokines, important in modulating metabolism and recently involved in intrauterine growth.This review aims to summarize reported findings concerning the role of adipocytokines (leptin, adiponectin, ghrelin, tumor necrosis factor (TNF), interleukin-6 (IL6), visfatin, resistin, apelin) in early life, while attempting to speculate mechanisms through which differential regulation of adipocytokines in IUGR may influence the risk for development of chronic diseases in later life.

Comparison of two models of intrauterine growth restriction for early catch-up growth and later development of glucose intolerance and obesity in rats

2010 ◽  
Vol 298 (1) ◽  
pp. R141-R146 ◽  
Author(s):  
Yasaman Shahkhalili ◽  
Julie Moulin ◽  
Irene Zbinden ◽  
Olivier Aprikian ◽  
Katherine Macé
Keyword(s):  
Body Weight ◽  
Birth Weight ◽  
Food Intake ◽  
Glucose Intolerance ◽  
Intrauterine Growth Restriction ◽  
Food Restriction ◽  
Plasma Insulin ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Catch Up

Two models of intrauterine growth restriction, maternal food restriction (FR), and dexamethasone (DEX) exposure were compared for early postnatal catch-up growth and later development of glucose intolerance and obesity in Sprague-Dawley rats. Mated dams were randomly divided into three groups at 10 days gestational age. Group FR was food restricted (50% of nongestating rats) during the last 11 days of gestation; Group DEX received DEX injections during the last week of gestation, and Group CON, the control group, had no intervention. Birth weight, catch-up growth, body weight, and food intake were measured in male offspring for 22 wk. Body composition, blood glucose, and plasma insulin in response to a glucose load were assessed at 8, 16, and 22 wk. Pups from both FR and DEX dams had similarly lower birth weights than CON (22% and 25%, P < 0.0001), but catch-up growth, which occurred during the suckling period, was much more rapid in FR than DEX offspring (6 vs. 25 days, 95% CI). Postweaning, there were no significant differences between groups in food intake, body weight, body fat, and plasma insulin, but baseline plasma glucose at 22 wk and 2-h glucose area-under-the-curve at 8 and 22 wk were greater only in FR vs. CON offspring ( P < 0.05), thereby contrasting with the lack of significant differences between DEX and CON. These results suggest that prenatal food restriction is a more sensitive model than DEX exposure for studies aimed at investigating the link between low birth weight, early postnatal catch-up growth, and later development of glucose intolerance.

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