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Am J Physiol Regul Integr Comp Physiol (November 11, 2004). doi:10.1152/ajpregu.00407.2004
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Submitted on June 18, 2004
Accepted on November 7, 2004

Hormonal regulation of glucose and system A amino acid transport in first trimester placental villous fragments

Anette Ericsson1*, Bengt Hamark2, Nina Jansson1, Bengt R Johansson3, Theresa L Powell1, and Thomas Jansson1

1 Perinatal Center, Physiology and Pharmacology, Gothenburg University, Gothenburg, Sweden
2 Obstetrics and Gynecology, Gothenburg University, Gothenburg, Sweden
3 Anatomy and Cell Biology, Gothenburg University, Gothenburg, Sweden

* To whom correspondence should be addressed. E-mail: anette.ericsson{at}fysiologi.gu.se.

Alterations in placental nutrient transfer have been implicated in fetal growth abnormalities. In pregnancies complicated by diabetes and accelerated fetal growth, up regulation of glucose transporter 1 (GLUT1) and amino acid transporter system A have been shown in the syncytiotrophoblast of term placenta. In contrast, intrauterine growth restriction is associated with a down-regulation of placental system A transporters. However, underlying mechanisms of transporter regulation are poorly understood, particularly in early pregnancy. In this study hormonal regulation of placental glucose and system A transporters was investigated. The uptake of 3-O-(methyl-14C)-D-glucose was studied in villous fragments isolated from first trimester (6-13 weeks of gestation) and term human placenta. Villous fragments were incubated in buffer containing insulin, leptin, cortisol, growth hormone (GH), prolactin, IGF-I or under hypo/hyperglycemic conditions for 1 h. Subsequently 3-O-(methyl-14C)-D-glucose uptake was measured with and without phloretin for 70 s in first trimester and 20 s in term tissue. MeAIB uptake was measured with and without Na+ for 20 min. Glucose uptake was unaltered by hormones or hypo/hyperglycemia. GH decreased system A activity by 31% in first trimester (p<0.05). The uptake of glucose was 50% higher in term as compared to first trimester fragments and increased markedly between 6-13 weeks of gestation (p<0.05). We conclude that placental glucose transporter activity is not regulated by short exposures to the hormones or glucose concentrations tested. In contrast to term placental villous fragments, system A activity was not regulated by insulin or leptin in first trimester but was down regulated by GH.




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