| Placental glucose and amino acid transport in calorie-restricted wild-type and Glut3 null heterozygous mice. | |
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MedLine Citation:
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PMID: 22700768 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Amit Ganguly; Laura Collis; Sherin U Devaskar |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2012-06-14 |
Journal Detail:
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Title: Endocrinology Volume: 153 ISSN: 1945-7170 ISO Abbreviation: Endocrinology Publication Date: 2012 Aug |
Date Detail:
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Created Date: 2012-07-23 Completed Date: 2012-10-01 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 0375040 Medline TA: Endocrinology Country: United States |
Other Details:
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Languages: eng Pagination: 3995-4007 Citation Subset: AIM; IM |
Affiliation:
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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. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Amino Acids
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metabolism* Animals Caloric Restriction* Female Glucose / metabolism* Glucose Transporter Type 1 / genetics, metabolism Glucose Transporter Type 3 / genetics, metabolism* Heterozygote Mice Placenta / metabolism* Pregnancy |
| Grant Support | |
ID/Acronym/Agency:
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HD 46979/HD/NICHD NIH HHS; HD-33997/HD/NICHD NIH HHS |
| Chemical | |
Reg. No./Substance:
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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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