Document Detail


Low protein diet fed exclusively during mouse oocyte maturation leads to behavioural and cardiovascular abnormalities in offspring.
MedLine Citation:
PMID:  18308825     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Early embryonic development is known to be susceptible to maternal undernutrition, leading to a disease-related postnatal phenotype. To determine whether this sensitivity extended into oocyte development, we examined the effect of maternal normal protein diet (18% casein; NPD) or isocaloric low protein diet (9% casein; LPD) restricted to one ovulatory cycle (3.5 days) prior to natural mating in female MF-1 mice. After mating, all females received NPD for the remainder of gestation and all offspring were litter size adjusted and fed standard chow. No difference in gestation length, litter size, sex ratio or postnatal growth was observed between treatments. Maternal LPD did, however, induce abnormal anxiety-related behaviour in open field activities in male and female offspring (P < 0.05). Maternal LPD offspring also exhibited elevated systolic blood pressure (SBP) in males at 9 and 15 weeks and in both sexes at 21 weeks (P < 0.05). Male LPD offspring hypertension was accompanied by attenuated arterial responsiveness in vitro to vasodilators acetylcholine and isoprenaline (P < 0.05). LPD female offspring adult kidneys were also smaller, but had increased nephron numbers (P < 0.05). Moreover, the relationship between SBP and kidney or heart size or nephron number was altered by diet treatment (P < 0.05). These data demonstrate the sensitivity of mouse maturing oocytes in vivo to maternal protein undernutrition and identify both behavioural and cardiovascular postnatal outcomes, indicative of adult disease. These outcomes probably derive from a direct effect of protein restriction, although indirect stress mechanisms may also be contributory. Similar and distinct postnatal outcomes were observed here compared with maternal LPD treatment during post-fertilization preimplantation development which may reflect the relative contribution of the paternal genome.
Authors:
Adam J Watkins; Adrian Wilkins; Colm Cunningham; V Hugh Perry; Meei J Seet; Clive Osmond; Judith J Eckert; Christopher Torrens; Felino R A Cagampang; Jane Cleal; William P Gray; Mark A Hanson; Tom P Fleming
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2008-02-28
Journal Detail:
Title:  The Journal of physiology     Volume:  586     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2008 Apr 
Date Detail:
Created Date:  2008-04-16     Completed Date:  2008-05-21     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  2231-44     Citation Subset:  IM    
Affiliation:
School of Biological Sciences, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, UK. ajw7@soton.ac.uk
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MeSH Terms
Descriptor/Qualifier:
Animals
Anxiety / metabolism*
Dietary Proteins / metabolism*
Female
Food Deprivation*
Hypertension / metabolism*
Mental Disorders / metabolism*
Mice
Oocytes / metabolism*
Pregnancy
Prenatal Exposure Delayed Effects*
Grant Support
ID/Acronym/Agency:
U01 HD044635/HD/NICHD NIH HHS; //British Heart Foundation
Chemical
Reg. No./Substance:
0/Dietary Proteins
Comments/Corrections

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