Glucose transporter isoform-3 mutations cause early pregnancy loss and fetal growth restriction

Ganguly, Amit; McKnight, Robert A.; Raychaudhuri, Santanu; Shin, Bo-Chul; Ma, Zhigui; Moley, Kelle; Devaskar, Sherin U.

doi:10.1152/ajpendo.00344.2006

Cited by 114

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Glucose transporter isoform-3 mutations cause early pregnancy loss and fetal growth restriction

Ganguly, Amit, McKnight, Robert A., Raychaudhuri, Santanu, Shin, Bo-Chul, Ma, Zhigui, Moley, Kelle, Devaskar, Sherin U.·2007·American Journal of Physiology-Endocrinology and Metabolism

DOI 10.1152/ajpendo.00344.2006

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Abstract

Glucose transporter isoform-3 (GLUT3) is the trophoblastic facilitative glucose transporter. To investigate the role of this isoform in embryonic development, we created a novel GLUT3-null mouse and observed arrested early embryonic development and loss at neurulation stage when both alleles were mutated. This loss occurred despite the presence of other related isoforms, particularly GLUT1. In contrast, when a single allele was mutated, despite increased embryonic cell apoptosis, adaptive changes in the subcellular localization of GLUT3 and GLUT1 in the preimplantation embryo led to postimplantation survival. This survival was compromised by decreased GLUT3-mediated transplacental glucose transport, causing late-gestation fetal growth restriction. This yielded young male and female adults demonstrating catch-up growth, with normal basal glucose, insulin, insulin-like growth factor-I and IGF-binding protein-3 concentrations, fat and lean mass, and glucose and insulin tolerance. We conclude that GLUT3 mutations cause a gene dose-dependent early pregnancy loss or late-gestation fetal growth restriction despite the presence of embryonic and placental GLUT1 and a compensatory increase in system A amino acid placental transport. This critical life-sustaining functional role for GLUT3 in embryonic development provides the basis for investigating the existence of human GLUT3 mutations with similar consequences during early pregnancy.

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Homozygous Glut3 deficient mice die prenatally.
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From Glucose transporter 3 is a rab11-dependent trafficking cargo and its transport to the cell surface is reduced in neurons of CAG140 Huntington’s disease mice (2014) · cites this paper as [41]

Adaptation of nutrient supply to fetal demand in the mouse involves interaction between the Igf2 gene and placental transporter systems
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“More recent studies in the IGF-II heterozygous null mouse demonstrated a decline in transplacental system A amino acid transfer to the fetus, with an adaptive increase in placental GLUT3-mediated transplacental glucose transport in response to fetal signals of impaired growth (7).”
Influential
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Sorted by citations

The SLC2 (GLUT) family of membrane transporters
Mueckler, M., & Thorens, B. (2013) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2012.07.001 · Cited by 1,328
The role of glucose transporters in brain disease: Diabetes and Alzheimer’s disease
Shah, K., DeSilva, S., & Abbruscato, T. (2012) · International Journal of Molecular Sciences · doi:10.3390/ijms131012629 · Cited by 288
Adaptations in placental phenotype support fetal growth during undernutrition of pregnant mice: Undernutrition and placental phenotype
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Copy-Number Variation of the Glucose Transporter Gene SLC2A3 and Congenital Heart Defects in the 22q11.2 Deletion Syndrome
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Glucose transporter 3 is a rab11-dependent trafficking cargo and its transport to the cell surface is reduced in neurons of CAG140 Huntington’s disease mice
McClory, H., Williams, D., Sapp, E., Gatune, L. W., Wang, P., DiFiglia, M., & Li, X. (2014) · Acta Neuropathologica Communications · doi:10.1186/s40478-014-0178-7 · Cited by 60
Placental Glucose and Amino Acid Transport in Calorie-Restricted Wild-Type and Glut3 Null Heterozygous Mice
Ganguly, A., Collis, L., & Devaskar, S. U. (2012) · Endocrinology · doi:10.1210/en.2011-1973 · Cited by 56
Self-citation
AMPK Knockdown in Placental Trophoblast Cells Results in Altered Morphology and Function
Carey, E. A. K., Albers, R. E., Doliboa, S. R., Hughes, M., Wyatt, C. N., Natale, D. R. C., & Brown, T. L. (2014) · Stem Cells and Development · doi:10.1089/scd.2014.0092 · Cited by 56

Authors: Ganguly, A., McKnight, R. A., Raychaudhuri, S., Shin, B.-C., Ma, Z., Moley, K., & Devaskar, S. U.
Venue: American Journal of Physiology-Endocrinology and Metabolism
Publisher: American Physiological Society
Published: 2007-05
Volume: 292
Issue: 5
Pages: E1241-E1255
ISSN: 0193-1849
1522-1555
DOI: 10.1152/ajpendo.00344.2006
Cited by: 114
References: 2
Language: en

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Glucose transporter isoform-3 mutations cause early pregnancy loss and fetal growth restriction

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