Glucose transporter gene expression in freshly isolated and cultured rat pneumocytes.

Abstract

Alveolar 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.