Document Detail


Epigenetic modification of fetal baboon hepatic phosphoenolpyruvate carboxykinase following exposure to moderately reduced nutrient availability.
MedLine Citation:
PMID:  20176628     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Decreased maternal nutrient availability during pregnancy induces compensatory fetal metabolic and endocrine responses. Knowledge of cellular changes involved is critical to understanding normal and abnormal development. Several studies in rodents and sheep report increased fetal plasma cortisol and associated increased gluconeogenesis in response to maternal nutrient reduction (MNR) but observations in primates are lacking. We determined MNR effects on fetal liver phosphoenolpyruvate carboxykinase 1 (protein, PEPCK1; gene, PCK1 orthologous/homologous human chromosomal region 20q13.31) at 0.9 gestation (G). Female baboon social groups were fed ad libitum (control, CTR) or 70% CTR (MNR) from 0.16 to 0.9G when fetuses were delivered by caesarean section under general anaesthesia. Plasma cortisol was elevated in fetuses of MNR mothers (P < 0.05). Immunoreactive PEPCK1 protein was located around the liver lobule central vein and was low in CTR fetuses but rose to 63% of adult levels in MNR fetuses. PCK1 mRNA measured by QRT-PCR increased in MNR (2.3-fold; P < 0.05) while the 25% rise in protein by Western blot analysis was not significant. PCK1 promoter methylation analysis using bisulfite sequencing was significantly reduced in six out of nine CpG-dinucleotides evaluated in MNR compared with CTR liver samples. In conclusion, these are the first data from a fetal non-human primate indicating hypomethylation of the PCK1 promoter in the liver following moderate maternal nutrient reduction.
Authors:
Mark J Nijland; Kozoh Mitsuya; Cun Li; Stephen Ford; Thomas J McDonald; Peter W Nathanielsz; Laura A Cox
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-02-22
Journal Detail:
Title:  The Journal of physiology     Volume:  588     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-04-16     Completed Date:  2010-07-29     Revised Date:  2013-09-02    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1349-59     Citation Subset:  IM    
Affiliation:
Center for Pregnancy and Newborn Research, University of Texas Health Science Center, San Antonio, TX, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Base Sequence
Epigenesis, Genetic / genetics,  physiology*
Female
Fetus / metabolism*
Liver / embryology*,  enzymology*
Malnutrition / metabolism*
Methylation
Models, Animal
Molecular Sequence Data
Papio / metabolism*
Phosphoenolpyruvate Carboxykinase (GTP) / genetics,  metabolism*
Pregnancy
RNA, Messenger / metabolism
Grant Support
ID/Acronym/Agency:
C06 RR013556/RR/NCRR NIH HHS; C06 RR015456/RR/NCRR NIH HHS; HD21350/HD/NICHD NIH HHS; P01 HD021350/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/RNA, Messenger; EC 4.1.1.32/Phosphoenolpyruvate Carboxykinase (GTP)
Comments/Corrections
Comment In:
J Physiol. 2010 May 1;588(Pt 9):1379-80   [PMID:  20436037 ]

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


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