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Am J Physiol Endocrinol Metab (January 9, 2007). doi:10.1152/ajpendo.00344.2006
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Submitted on July 13, 2006
Accepted on January 1, 2007

Glucose Transporter Isoform 3 Mutations Cause Early Pregnancy Loss and Fetal Growth Restriction

Amit Ganguly1, Robert A. McKnight1, Santanu Raychaudhuri1, Bo-Chul Shin1, Zhigui Ma1, Kelle Moley2, and Sherin Uday Devaskar1*

1 Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, California, United States
2 Obstetrics and Gynecology, Cell Biology and Physiology, Washingon University School of Medicine, St. Louis, Missouri, United States

* To whom correspondence should be addressed. E-mail: sdevaskar{at}mednet.ucla.edu.

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 sub-cellular localization of GLUT3 and GLUT1 in the pre-implantation embryo led to post-implantation survival. This survival was compromised by decreased GLUT3 mediated trans-placental 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 1 and IGF-binding protein 3 concentrations, fat and lean mass, and glucose and insulin tolerance. We conclude that glucose transporter isoform 3 (GLUT3) mutations cause a gene dose dependent early pregnancy loss or late gestation fetal growth restriction, despite the presence of embryonic and placental glucose transporter isoform 1 (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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