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Cited by 56Birth, Development, and HealthPregnancy and preeclampsia studiesMetabolism, Diabetes, and Cancer

Placental Glucose and Amino Acid Transport in Calorie-Restricted Wild-Type and Glut3 Null Heterozygous Mice

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Ganguly, Amit, Collis, Laura, Devaskar, Sherin U.·2012·Endocrinology
DOI 10.1210/en.2011-1973PMC PMC3404359
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Abstract

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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  • A 20% reduction in food intake for most of mouse pregnancy up-regulates amino acid transport per gram of placenta in association with relatively small reductions in fetal-placental weight close to term.

    “For example, a 50% reduction in food intake for the second half of mouse pregnancy leads to reduced placental glucose and amino acid delivery and severe feto-placental growth restriction, whereas a 20% reduction in food intake for most of pregnancy up-regulates amino acid transport per gram of placenta in association with relatively small reductions in fetal-placental weight close to term (120, 20”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [207]

  • A 50% reduction in food intake for the second half of mouse pregnancy leads to reduced placental glucose and amino acid delivery and severe feto-placental growth restriction.

    “For example, a 50% reduction in food intake for the second half of mouse pregnancy leads to reduced placental glucose and amino acid delivery and severe feto-placental growth restriction, whereas a 20% reduction in food intake for most of pregnancy up-regulates amino acid transport per gram of placenta in association with relatively small reductions in fetal-placental weight close to term (120, 20”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [207]

  • When the placental supply of glucose to the fetus is disrupted by deletion of the Slc2a3 gene, the placenta compensates by upregulating placental amino acid transport and transporter expression sufficiently to maintain normal fetal growth and metabolism until term.

    “Similarly, when the placental supply of glucose to the fetus is disrupted by deletion of the Slc2a3 gene, the placenta compensates by upregulating placental amino acid transport and transporter expression sufficiently to maintain normal fetal growth and metabolism until term (207).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [207]

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Authors
Ganguly, A., Collis, L., & Devaskar, S. U.
Affiliations
University of California, Los Angeles (US)
Corresponding author
Devaskar, Sherin U.
ORCID
Devaskar, Sherin U.
Venue
Endocrinology
Publisher
The Endocrine Society
Published
2012-06-14
Volume
153
Issue
8
Pages
3995-4007
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
DOI
10.1210/en.2011-1973
PMC
PMC3404359
OpenAlex
W1996100153
Cited by
56
References
42
Citations by year
2024: 3 · 2023: 2 · 2022: 4 · 2021: 5 · 2020: 3 · 2019: 4 · 2018: 7 · 2017: 4 · 2016: 9 · 2015: 5 · 2014: 4 · 2013: 6
FWCI
4.21
Type
journal article
Language
en
Open access
Locations
  • Endocrinology (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-33997, HD46979, R01HD033997, R01HD046979)
Topics
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords
placental glucose transport, placental amino acid transport, caloric restriction, GLUT3, leucine transport, system A amino acid transport, SNAT2, LAT2, GLUT1, mTOR signaling, p70 S6 kinase, 4E-binding protein 1, fetal growth, placenta
MeSH terms
Amino Acids, Animals, Female, Glucose, Heterozygote, Placenta, Pregnancy, Caloric Restriction, Glucose Transporter Type 1, Glucose Transporter Type 3, Mice

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