Document Detail

Cardio-renal and metabolic adaptations during pregnancy in female rats born small: implications for maternal health and second generation fetal growth.
MedLine Citation:
PMID:  22144579     Owner:  NLM     Status:  MEDLINE    
Intrauterine growth restriction caused by uteroplacental insufficiency increases risk of cardiovascular and metabolic disease in offspring. Cardio-renal and metabolic responses to pregnancy are critical determinants of immediate and long-term maternal health. However, no studies to date have investigated the renal and metabolic adaptations in growth restricted offspring when they in turn become pregnant. We hypothesised that the physiological challenge of pregnancy in growth restricted females exacerbates disease outcome and compromises next generation fetal growth. Uteroplacental insufficiency was induced by bilateral uterine vessel ligation (Restricted) or sham surgery (Control) on day 18 of gestation in WKY rats and F1 female offspring birth and postnatal body weights were recorded. F1 Control and Restricted females were mated at 4 months and blood pressure, renal and metabolic parameters were measured in late pregnancy and F2 fetal and placental weights recorded. Age-matched non-pregnant Control and Restricted F1 females were also studied. F1 Restricted females were born 10-15% lighter than Controls. Basal insulin secretion and pancreatic β-cell mass were reduced in non-pregnant Restricted females but restored in pregnancy. Pregnant Restricted females, however, showed impaired glucose tolerance and compensatory glomerular hypertrophy, with a nephron deficit but normal renal function and blood pressure. F2 fetuses from Restricted mothers exposed to physiological measures during pregnancy were lighter than Controls highlighting additive adverse effects when mothers born small experience stress during pregnancy. Female rats born small exhibit mostly normal cardio-renal adaptations but altered glucose control during late pregnancy making them vulnerable to lifestyle challenges.
Linda A Gallo; Melanie Tran; Karen M Moritz; Marc Q Mazzuca; Laura J Parry; Kerryn T Westcott; Andrew J Jefferies; Luise A Cullen-McEwen; Mary E Wlodek
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-12-05
Journal Detail:
Title:  The Journal of physiology     Volume:  590     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-02-02     Completed Date:  2012-06-21     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  617-30     Citation Subset:  IM    
Department of Physiology, The University of Melbourne, Parkville, VIC 3010, Australia.
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MeSH Terms
Blood Glucose / analysis
Body Weight
Fetal Growth Retardation / pathology,  physiopathology*
Heart / growth & development
Insulin / blood
Kidney / pathology,  physiology
Organ Size
Pancreas / growth & development,  pathology
Placental Insufficiency / pathology,  physiopathology
Rats, Inbred WKY
Uterus / growth & development
Reg. No./Substance:
0/Blood Glucose; 0/Insulin
Comment In:
J Physiol. 2012 Mar 1;590(Pt 5):1019   [PMID:  22399819 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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