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pubmed-article:11982500pubmed:abstractTextAlveolar epithelium in situ takes up luminal glucose by cotransport with sodium. Cultured alveolar type II pneumocytes have only sodium-independent glucose uptake. It is unclear which isoforms are responsible for glucose transport in these cells and why sodium-glucose cotransport activity disappears during culture. GLUT1, GLUT4, GLUT5 and SGLT1 mRNA were detected in freshly isolated rat alveolar type II cells by reverse transcriptase-polymerase chain reaction. We show that SGLT1 mRNA was 90% lower in cells cultured in plastic wells for 2 or 4 days than in freshly isolated cells. mRNAs coding for the facilitated transporters were reduced from 40% (GLUT1) and 75% (GLUT4 and GLUT5) in cultured cells. Cells cultured at the air-liquid interface better preserved their phenotype as attested by significantly higher surfactant-associated protein mRNA levels. However, these cells had no higher GLUT1 and SGLT1 gene expression. Thus, alveolar type II cells lose sodium-glucose cotransport activity in part because of a decrease in mRNA levels. These changes in gene expression and/or mRNA stability may be an additional consequence of the shift towards the type I cell phenotype observed in cultured type II pneumocytes.lld:pubmed
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pubmed-article:11982500pubmed:dateRevised2005-11-17lld:pubmed
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pubmed-article:11982500pubmed:articleTitleGlucose transporter gene expression in freshly isolated and cultured rat pneumocytes.lld:pubmed
pubmed-article:11982500pubmed:affiliationINSERM U82, Faculté Xavier Bichat, Paris, France.lld:pubmed
pubmed-article:11982500pubmed:publicationTypeJournal Articlelld:pubmed
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