Document Detail


Acute supplementation of amino acids increases net protein accretion in IUGR fetal sheep.
MedLine Citation:
PMID:  22649066     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Placental insufficiency decreases fetal amino acid uptake from the placenta, plasma insulin concentrations, and protein accretion, thus compromising normal fetal growth trajectory. We tested whether acute supplementation of amino acids or insulin into the fetus with intrauterine growth restriction (IUGR) would increase net fetal protein accretion rates. Late-gestation IUGR and control (CON) fetal sheep received acute, 3-h infusions of amino acids (with euinsulinemia), insulin (with euglycemia and euaminoacidemia), or saline. Fetal leucine metabolism was measured under steady-state conditions followed by a fetal muscle biopsy to quantify insulin signaling. In CON, increasing amino acid delivery rates to the fetus by 100% increased leucine oxidation rates by 100%. In IUGR, amino acid infusion completely suppressed fetal protein breakdown rates but increased leucine oxidation rate by only 25%, resulting in increased protein accretion rates by 150%. Acute insulin infusion, however, had very little effect on amino acid delivery rates, fetal leucine disposal rates, or fetal protein accretion rates in CON or IUGR fetuses despite robust signaling of the fetal skeletal muscle insulin-signaling cascade. These results indicate that, when amino acids are given directly into the fetal circulation independently of changes in insulin concentrations, IUGR fetal sheep have suppressed protein breakdown rates, thus increasing net fetal protein accretion.
Authors:
Laura D Brown; Paul J Rozance; Stephanie R Thorn; Jacob E Friedman; William W Hay
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Publication Detail:
Type:  Comparative Study; Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-05-29
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  303     ISSN:  1522-1555     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-08-02     Completed Date:  2012-10-17     Revised Date:  2013-08-14    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E352-64     Citation Subset:  IM    
Affiliation:
Perinatal Research Center, Department of Pediatrics, University of Colorado School of Medicine, Aurora, CO 80045, USA. laura.brown@ucdenver.edu
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MeSH Terms
Descriptor/Qualifier:
Amino Acids / administration & dosage*,  pharmacokinetics
Animals
Carbon Isotopes / administration & dosage,  pharmacokinetics
Dietary Supplements
Disease Models, Animal*
Female
Fetal Growth Retardation / metabolism*,  pathology
Insulin / administration & dosage
Leucine / administration & dosage,  pharmacokinetics
Pregnancy
Protein Biosynthesis / drug effects,  physiology
Proteins / metabolism*
Proteolysis / drug effects
Random Allocation
Sheep*
Time Factors
Grant Support
ID/Acronym/Agency:
DK-52138/DK/NIDDK NIH HHS; HD-07186/HD/NICHD NIH HHS; K01 DK-090199/DK/NIDDK NIH HHS; K01 DK090199/DK/NIDDK NIH HHS; K08 HD-060688/HD/NICHD NIH HHS; K08 HD060688/HD/NICHD NIH HHS; K12 HD-057022/HD/NICHD NIH HHS; P30 DK-57516/DK/NIDDK NIH HHS; R01 DK-088139/DK/NIDDK NIH HHS; R01 DK088139/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Amino Acids; 0/Carbon Isotopes; 0/Insulin; 0/Proteins; 61-90-5/Leucine
Comments/Corrections

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


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