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Aortic endothelial cells transport more glucose than pulmonary endothelial cells in vitro
Author(s) -
Viator Ryan Joseph,
Fouty Brian William
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.856.11
Subject(s) - glucose transporter , medicine , endothelial dysfunction , diabetes mellitus , glucose uptake , endocrinology , insulin resistance , insulin , endothelial stem cell , intracellular , western blot , stress hyperglycemia , in vitro , chemistry , biology , microbiology and biotechnology , biochemistry , gene
Diabetes is characterized by hyperglycemia resulting from insulin resistance or deficiency. Increases in intracellular glucose can lead to endothelial dysfunction. While systemic vascular disease is a major cause of morbidity and mortality in diabetics, pulmonary vascular disease is less clinically apparent. Since both circulations are exposed to similar circulating glucose and insulin concentrations, we hypothesize that increased glucose loading of systemic endothelial cells might explain this difference. Using bovine aortic and pulmonary artery endothelial cells from the same animal (AECs or PAECs, respectively), we found that AECs transported 5‐fold more glucose than PAECs. Because shear stress is different between the two vascular beds, we examined the effect of shear stress on glucose transport. Flow adapted cells decreased radiolabelled glucose uptake but remained higher in AECs. Glucose enters endothelial cells primarily through the glucose transporter, Glut‐1. To determine if an increase in Glut‐1 expression might explain the difference in glucose uptake, we compared cells using Western Blot Analysis. AECs expressed more Glut‐1 than the PAECs. The increased glucose loading of AECs compared to PAECs may be important in determining the different effects of diabetes in the systemic and pulmonary circulations. This research is supported by the NIH grants R01HL070273 and T32HL076125.