Document Detail


Impaired placental nutrient transport in mice generated by in vitro fertilization.
MedLine Citation:
PMID:  22562173     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
More than 4.5 million children have been conceived by in vitro fertilization (IVF). Interestingly, singleton IVF offspring born at term have an increased incidence of low birth weight. The mechanism responsible for the lower birth weight is unknown, but alterations in placental function are possible. Hence, the goal of our study was to examine placental growth and function in mice generated in vivo or in vitro. To assess placental function, blastocysts were generated by IVF or produced by natural mating (control group); both IVF and control blastocysts were transferred to pseudopregnant recipients. Placental weights did not differ at embryonic d 15.5 (E15.5) but were increased at E18.5 in the IVF group (25.4%, P < 0.001) compared with control. Proliferation was increased in IVF placentae, whereas overall placental gross morphology and apoptosis were not affected. Both fetal weights (16.4% lower at E15.5 and 8.8% lower at E18.5, P < 0.05) and fetal to placental ratios were lower (P < 0.001) in the IVF compared with the control group at both time points, whereas birth weights did not differ. At E18.5, the mRNA for selected glucose, system A amino acid transporters, and imprinted genes were down-regulated in IVF placentae. GLUT3 protein level was decreased in the IVF group (P < 0.05). Importantly, intrajugular injections of (14)C-methyl-D-glucose or (14)C-MeAIB tracers (n = 6 litters per group) showed that placental transport of glucose and amino acids were 24.8% (not significant) and 58.1% (P < 0.05) lower in the IVF group. Fetal accumulation of glucose was not different, but amino acid accumulation was significantly (36 %) lower in IVF fetuses (P < 0.05). We conclude that IVF alters both fetal and placental growth and, importantly, decreases placental transport efficiency in mice conceived by IVF.
Authors:
Enrrico Bloise; Wingka Lin; Xiaowei Liu; Rhodel Simbulan; Kevin S Kolahi; Felice Petraglia; Emin Maltepe; Annemarie Donjacour; Paolo Rinaudo
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-05-04
Journal Detail:
Title:  Endocrinology     Volume:  153     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-06-25     Completed Date:  2012-09-20     Revised Date:  2013-07-02    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3457-67     Citation Subset:  AIM; IM    
Affiliation:
Department of Obstetrics Gynecology and Reproductive Science, University of California, San Francisco, 513 Parnassus Avenue, San Francisco, California 94143-0916, USA.
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MeSH Terms
Descriptor/Qualifier:
Amino Acids / metabolism
Animals
Apoptosis
Biological Transport
Blastocyst / metabolism
Embryo Transfer
Female
Fertilization in Vitro / methods*
Fetal Weight
Glucose / metabolism
Mice
Models, Animal
Organ Size
Placenta / metabolism,  physiology*
Pregnancy
Pregnancy, Animal
Time Factors
Grant Support
ID/Acronym/Agency:
NICHD R01 062803-01A1//PHS HHS
Chemical
Reg. No./Substance:
0/Amino Acids; 50-99-7/Glucose
Comments/Corrections

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