Document Detail


Preimplantation exposure of mouse embryos to palmitic acid results in fetal growth restriction followed by catch-up growth in the offspring.
MedLine Citation:
PMID:  21653893     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Free fatty acids (FFAs) are energy substrates for many cell types, but in excess, some FFAs can accumulate in nonadipose cells, inducing apoptosis. Also known as lipotoxicity, this phenomenon may play a role in the development of obesity-related disease. Obesity is common among reproductive age women and is associated with adverse pregnancy and fetal outcomes; however, little is known about the effects of excess FFAs on embryos and subsequent fetal development. To address this knowledge gap, murine blastocysts were cultured in excess palmitic acid (PA), the most abundant saturated FFA in human serum, and ovarian follicular fluid. Targets susceptible to aberrations in maternal physiology, including embryonic IGF1 receptor (IGF1R) expression, glutamic pyruvate transaminase (GPT2) activity, and nuclei count, were measured. PA-exposed blastocysts demonstrated altered IGF1R expression, increased GPT2 activity, and decreased nuclei count. Trophoblast stem cells derived from preimplantation embryos were also cultured in PA. Cells exposed to increasing doses of PA demonstrated increased apoptosis and decreased proliferation. To demonstrate long-term effects of brief PA exposure, blastocysts cultured for 30 h in PA were transferred into foster mice, and pregnancies followed through Embryonic Day (ED)14.5 or delivery. Fetuses resulting from PA-exposed blastocysts were smaller than controls at ED14.5. Delivered pups were also smaller but demonstrated catch-up growth and ultimately surpassed control pups in weight. Altogether, our data suggest brief PA exposure results in altered embryonic metabolism and growth, with lasting adverse effects on offspring, providing further insight into the pathophysiology of maternal obesity.
Authors:
Emily S Jungheim; Erica D Louden; Maggie M-Y Chi; Antonina I Frolova; Joan K Riley; Kelle H Moley
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-06-08
Journal Detail:
Title:  Biology of reproduction     Volume:  85     ISSN:  1529-7268     ISO Abbreviation:  Biol. Reprod.     Publication Date:  2011 Oct 
Date Detail:
Created Date:  2011-10-03     Completed Date:  2012-02-15     Revised Date:  2014-09-08    
Medline Journal Info:
Nlm Unique ID:  0207224     Medline TA:  Biol Reprod     Country:  United States    
Other Details:
Languages:  eng     Pagination:  678-83     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis
Blastocyst / cytology,  metabolism*
Body Weight
Cell Count
Cell Proliferation
Cells, Cultured
Crosses, Genetic
Ectogenesis
Embryo Transfer
Female
Fetal Development*
Fetal Growth Retardation / etiology*
Fetus / metabolism
Insulin-Like Growth Factor I / metabolism
Male
Mice
Obesity / etiology*
Palmitic Acid / adverse effects*
Pregnancy
Transaminases / metabolism
Trophoblasts / cytology,  metabolism
Grant Support
ID/Acronym/Agency:
K12HD-063086-01/HD/NICHD NIH HHS; NSO57105//PHS HHS; P30 DK056341/DK/NIDDK NIH HHS; P30 DK056341-11/DK/NIDDK NIH HHS; R01 HD040390/HD/NICHD NIH HHS; R01-DK070351/DK/NIDDK NIH HHS; T32-HD-07440-07/HD/NICHD NIH HHS; U01HD-044691/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/insulin-like growth factor-1, mouse; 2V16EO95H1/Palmitic Acid; 67763-96-6/Insulin-Like Growth Factor I; EC 2.6.1.-/Transaminases; EC 2.6.1.15/glutamine-pyruvate aminotransferase
Comments/Corrections

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


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