Document Detail

Placental glucose and amino acid transport in calorie-restricted wild-type and Glut3 null heterozygous mice.
MedLine Citation:
PMID:  22700768     Owner:  NLM     Status:  MEDLINE    
Calorie restriction (CR) decreased placenta and fetal weights in wild-type (wt) and glucose transporter (Glut) 3 heterozygous null (glut3(+/-)) mice. Because placental nutrient transport is a primary energy determinant of placentofetal growth, we examined key transport systems. Maternal CR reduced intra- and transplacental glucose and leucine transport but enhanced system A amino acid transport in wt mice. These transport perturbations were accompanied by reduced placental Glut3 and leucine amino acid transporter (LAT) family member 2, no change in Glut1 and LAT family member 1, but increased sodium coupled neutral amino acid transporter (SNAT) and SNAT2 expression. We also noted decreased total and active phosphorylated forms of mammalian target of rapamycin, which is the intracellular nutrient sensor, the downstream total P70S6 kinase, and pS6 ribosomal protein with no change in total and phosphorylated 4E-binding protein 1. To determine the role of placental Glut3 in mediating CR-induced placental transport changes, we next investigated the effect of gestational CR in glut3(+/-) mice. In glut3(+/-) mice, a key role of placental Glut3 in mediating transplacental and intraplacental glucose transport was established. In addition, reduced Glut3 results in a compensatory increase of leucine and system A transplacental transport. On the other hand, diminished Glut3-mediated intraplacental glucose transport reduced leucine transport and mammalian target of rapamycin and preserved LAT and enhancing SNAT. CR in glut3(+/-) mice further reduced transplacental glucose transport and enhanced system A amino acid transport, although the increased leucine transport was lost. In addition, increased Glut3 was seen and preserved Glut1, LAT, and SNAT. These placental changes collectively protect survival of wt and glut3(+/-) fetuses against maternal CR-imposed reduction of macromolecular nutrients.
Amit Ganguly; Laura Collis; Sherin U Devaskar
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-06-14
Journal Detail:
Title:  Endocrinology     Volume:  153     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-07-23     Completed Date:  2012-10-01     Revised Date:  2013-08-13    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3995-4007     Citation Subset:  AIM; IM    
Division of Neonatology and Developmental Biology, Neonatal Research Center, Department of Pediatrics, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California 90095-1752, USA.
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MeSH Terms
Amino Acids / metabolism*
Caloric Restriction*
Glucose / metabolism*
Glucose Transporter Type 1 / genetics,  metabolism
Glucose Transporter Type 3 / genetics,  metabolism*
Placenta / metabolism*
Grant Support
Reg. No./Substance:
0/Amino Acids; 0/Glucose Transporter Type 1; 0/Glucose Transporter Type 3; 0/Slc2a1 protein, mouse; 0/Slc2a3 protein, mouse; 50-99-7/Glucose

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