Authors: María Noel Galardo María Fernanda Riera Eliana Herminia Pellizzari Héctor Edgardo Chemes Marcela Cristina Venara Selva Beatriz Cigorraga Silvina Beatriz Meroni
Publish Date: 2008/09/19
Volume: 334, Issue: 2, Pages: 295-
Abstract
Sertoli cells are necessary to provide adequate levels of lactate for germ cell development Lactate production is hormonally regulated by folliclestimulating hormone FSH and by a large set of intratesticular regulators such as interleukin1β IL1β and basic fibroblast growth factor bFGF Little is known regarding the critical step in the production of this metabolite viz the entrance of glucose into the cell as mediated by GLUTs The aim of the present study was to investigate the expression of the glucose transporters GLUT1 and GLUT3 and its possible regulation by FSH IL1β and bFGF in Sertoli cells at two different timepoints in sexual development Sertoli cells retaining the ability to undergo mitosis obtained from 8dayold rats and in the process of terminal differentiation obtained from 20dayold rats were examined Testicular tissue sections and Sertoli cell monolayers obtained from 8 and 20dayold rats showed positive immunostaining for GLUT1 and GLUT3 proteins GLUT1 and GLUT3 mRNA levels were detected at the two ages analyzed Treatment of Sertoli cells obtained from 8 and 20dayold rats with FSH IL1β and bFGF for various periods of time 12 24 and 48 h increased GLUT1 without changing GLUT3 mRNA levels Our results thus show that Sertoli cells express GLUT1 and GLUT3 throughout pubertal development and that in Sertoli cells only GLUT1 is regulated by hormones during pubertal development Hormonal regulation of GLUT1 expression and consequently glucose uptake and lactate production may be a key molecular event in the regulation of spermatogenesis by hormonesThe work was supported by grants from the Agencia Nacional de Promoción Científica y Tecnológica PICT 25365 and CONICET PIP 5479 Argentina RMF CHE CSB and MSB are established investigators of CONICET GMN is a recipient of a CONICET fellowship and a teaching assistant of Departamento de Bioquímica Humana Facultad de Medicina UBAThe authors express their gratitude to Dr Birnbaum Philadelphia USA for providing GLUT1 cDNA to Dr Nagamatsu Tokyo Japan for providing GLUT3 cDNA and to Dr CarterSu Michigan USA for providing the GLUT1 antibody The technical help of Mercedes Astarloa is also gratefully acknowledged
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