Document Detail


Effects of maternal global nutrient restriction on fetal baboon hepatic insulin-like growth factor system genes and gene products.
MedLine Citation:
PMID:  19574404     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Knowledge of altered maternal nutrition effects on growth-regulating systems is critical to understanding normal and abnormal fetal development. There are many reports of hepatic fetal IGF system responses to maternal nutrient restriction (MNR) during pregnancy in rodents and sheep but none in nonhuman primates. We determined effects of MNR on the fetal baboon hepatic IGF system. Social groups of female baboons were fed ad libitum, controls, or 70% controls (MNR) from 0.16 to 0.5 gestation and fetuses delivered by cesarean section. Fetal liver tissue was analyzed for IGF-I, IGF-II, and IGF binding protein (IGFBP)-3 mRNA by in situ hybridization and quantitative RT-PCR and protein by immunohistochemistry (IHC); IGF-I receptor, IGF-II receptor by quantitative RT-PCR and IHC and IGFBP-1 by in situ hybridization and IHC. MNR did not alter fetal body or liver weight. Fetal hepatic glycogen staining increased with MNR. MNR reduced fetal hepatic IGF-I and IGF-II and increased IGFBP-1 mRNA and decreased IGF-I, IGF-II, IGF-I receptor, and IGF-II receptor protein and increased protein for IGFBP-1 and IGFBP-3. MNR increased caspase-3, indicating apoptosis and decreased Akt staining, indicating decreased nutrient sensing. In conclusion, whereas fetal body and liver weights did not change in response to moderate MNR during the first half of baboon pregnancy, the major indices of function of the hepatic IGF system measured were all reduced.
Authors:
Cun Li; Natalia E Schlabritz-Loutsevitch; Gene B Hubbard; Victor Han; Karen Nygard; Laura A Cox; Thomas J McDonald; Peter W Nathanielsz
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2009-07-02
Journal Detail:
Title:  Endocrinology     Volume:  150     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2009 Oct 
Date Detail:
Created Date:  2009-09-22     Completed Date:  2009-10-22     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4634-42     Citation Subset:  AIM; IM    
Affiliation:
Center for Pregnancy and Newborn Research, University of Texas Health Science Center at San Antonio, Texas 78229, USA. lic@uthscsa.edu
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MeSH Terms
Descriptor/Qualifier:
Amniotic Fluid / metabolism
Animals
Brain / metabolism
Caspase 3 / metabolism
Female
Fetal Development
Fetus / metabolism*
Insulin-Like Growth Factor Binding Protein 1 / metabolism
Insulin-Like Growth Factor Binding Protein 3 / metabolism
Ki-67 Antigen / metabolism
Kidney / metabolism
Liver / growth & development,  metabolism*
Liver Glycogen / metabolism
Nutritional Status*
Organ Size
Papio
Placenta / growth & development,  metabolism
Pregnancy / physiology*
Proto-Oncogene Proteins c-akt / metabolism
RNA, Messenger / metabolism
Receptor, IGF Type 1 / metabolism
Receptor, IGF Type 2 / metabolism
Reverse Transcriptase Polymerase Chain Reaction
Somatomedins / genetics,  metabolism*
Grant Support
ID/Acronym/Agency:
HD 21350/HD/NICHD NIH HHS; P01 HD 21350/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Insulin-Like Growth Factor Binding Protein 1; 0/Insulin-Like Growth Factor Binding Protein 3; 0/Ki-67 Antigen; 0/Liver Glycogen; 0/RNA, Messenger; 0/Receptor, IGF Type 2; 0/Somatomedins; EC 2.7.10.1/Receptor, IGF Type 1; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 3.4.22.-/Caspase 3
Comments/Corrections

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


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