scholarly journals OP20.03: Difference of postnatal catch-up growth in fetuses with intrauterine growth restriction according to the maternal hypertensive disease

2011 ◽  
Vol 38 (S1) ◽  
pp. 113-114
Author(s):  
S. Kim ◽  
J. Jun ◽  
C. Park ◽  
J. Park ◽  
H. C. Syn
Keyword(s):  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Hypertensive Disease ◽  
Intrauterine Growth ◽  
Catch Up

The timing of “catch-up growth” affects metabolism and appetite regulation in male rats born with intrauterine growth restriction

2009 ◽  
Vol 297 (3) ◽  
pp. R813-R824 ◽  
Author(s):  
Bérengère Coupé ◽  
Isabelle Grit ◽  
Dominique Darmaun ◽  
Patricia Parnet
Keyword(s):  
Feeding Behavior ◽  
Intrauterine Growth Restriction ◽  
Rest Period ◽  
Metabolic Programming ◽  
Growth Restriction ◽  
Male Rats ◽  
Chow Diet ◽  
Adult Age ◽  
Intrauterine Growth ◽  
Catch Up

Epidemiological studies demonstrated a relationship between low birth weight mainly caused by intrauterine growth restriction (IUGR) and adult metabolic disorders. The concept of metabolic programming centers on the idea that nutritional and hormonal status during the key period of development determines the long-term control of energy balance by programming future feeding behavior and energy expenditure. The present study examined the consequence of early or late “catch-up growth” after IUGR on feeding behavior and metabolic cues of male offspring of rat dams exposed to protein restriction during gestation and/or lactation. Our results suggest that early catch-up growth may be favorable for fasting metabolic parameters at weaning, as no differences were observed on plasma leptin, triglyceride, glucose, and insulin levels compared with controls. In contrast, if pups remained malnourished until weaning, low insulin concentration was detected and was accompanied by hyperphagia associated with a large increase in hypothalamic NPY and AgRP mRNA expression. At adult age, on a regular chow diet, only the meal structure was modified by fetal programming. The two IUGR groups demonstrated a reduced meal duration that enhanced the speed of food ingestion and consequently increased the rest period associated to the satiety state without changes in the hypothalamic expression of appetite neuropeptides. Our findings demonstrate that in IUGR, regardless of postnatal growth magnitude, metabolic programming occurred in utero and was responsible for both feeding behavior alteration and postprandial higher insulin level in adults. Additionally, catch-up growth immediately after early malnutrition could be a key point for the programming of postprandial hyperleptinemia.

scholarly journals Influence of catch up growth on spatial learning and memory in a mouse model of intrauterine growth restriction

PLoS ONE ◽  
2017 ◽  
Vol 12 (5) ◽  
pp. e0177468 ◽  
Author(s):  
Cristina Duran Fernandez-Feijoo ◽  
Cristina Carrasco Carrasco ◽  
Núria Villalmazo Francisco ◽  
Judit Cebrià Romero ◽  
Jose Ramon Fernández Lorenzo ◽  
...  
Keyword(s):  
Mouse Model ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Spatial Learning And Memory ◽  
Intrauterine Growth ◽  
Catch Up

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.

Abstract TMP120: Genetic, Environmental and Stochastic Factors Contribute to Variation in the Posterior Communicating Collaterals of the Circle of Willis

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
James E Faber ◽  
Wojciech Rzechorzek ◽  
Kathy Z Dai ◽  
Benjamin T Summers ◽  
Cooper N Blazek ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Genetic Background ◽  
Tissue Injury ◽  
Developmental Differences ◽  
Growth Restriction ◽  
Mouse Strains ◽  
Stochastic Variation ◽  
Intrauterine Growth ◽  
Collateral Arteries ◽  
Catch Up

Variation in blood flow mediated by the posterior communicating collateral arteries (PComs) contributes to variation in severity of tissue injury in obstructive disease. The “extent” of PCom collaterals (lumen diameter &/or number—ie, presence bilaterally, unilaterally or absent) varies widely in humans and other species due in part to developmental differences, since well-known patterns of variation are present at birth. However, mechanisms underlying this variation have not been examined. Herein we used angiography to probe involvement of genetic, environmental and stochastic factors. PCom extent varied widely among 7 mouse strains with different genetic backgrounds that was unrelated to differences in PCA diameter or brain weight. The pattern differed strongly from that previously reported by us for differences in extent of pial collateral arterioles. Like pial collaterals, PCom diameter was reduced by advanced aging (-28±3%, n=11-16, p<0.01; opposite seen for PCA diameter) and hypertension (-14±8%, n=7-9, p<0.05; -18% for PCA diameter). In contrast to pial collaterals, obesity, hyperlipidemia, metabolic syndrome and diabetes had no effect on PCom extent (or PCA diameter). Intrauterine growth restriction reduced PCom diameter 55±4% (n=6-17, p<0.05; -24% for PCA) in the adult despite catch-up growth of brain after birth, while pial collaterals were unaffected. Compared to pial collaterals (and PCA), PCom extent evidenced >8-fold larger stochastic variation (n=16, p<0.01). In addition, PComs underwent outward remodeling after MCA occlusion that varied with genetic background (12-133% lumen enlargement among 5 strains; n=5-14, p<0.05-0.001) and was greater on the side of occlusion in most strains. In conclusion, variation in number and diameter of PCom collateral arteries arises from genetic, environmental and stochastic factors. The responsible genetic polymorphisms appear to differ from those that contribute to variation in extent of pial collateral arterioles. Extent of PComs is also adversely affected by intrauterine growth restriction, aging and hypertension. These findings suggest possible sources of PCom variation in humans and provide information relevant when studying mouse models of occlusive cerebrovascular disease.

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