Regulation of insulin-stimulated glucose transport by chronic glucose exposure in 3T3-L1 adipocytes

Citation
T. Hosaka et al., Regulation of insulin-stimulated glucose transport by chronic glucose exposure in 3T3-L1 adipocytes, ENDOCR J, 46(3), 1999, pp. 349-357
Citations number
29
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
ENDOCRINE JOURNAL
ISSN journal
0918-8959 → ACNP
Volume
46
Issue
3
Year of publication
1999
Pages
349 - 357
Database
ISI
SICI code
0918-8959(199906)46:3<349:ROIGTB>2.0.ZU;2-9
Abstract
Chronic hyperglycemia causes insulin resistance, termed glucose toxicity. H erein we studied chronic glucose-dependent regulation of the glucose transp ort system in adipocytes. 3T3-L1 adipocytes were incubated for up to 24 h w ith low (1 mM) or high (25 mM) glucose, and glucose transport was subsequen tly analyzed. 100 nM insulin was present throughout the experiments. 24 h i ncubation with 1 mM glucose caused a 2.3 +/- 0.4 fold increase in glucose t ransport activity, compared to the values obtained with 25 mM glucose. This difference was not observed when 24 h incubation was carried out without i nsulin. Glucose transport activity was not increased at 3 or 6 h incubation with 1 mM glucose, but was increased at 12 h, which closely paralleled inc reased expression of GLUT1. In addition to increased GLUT1 expression, more efficient translocation of GLUT1 to the plasma membrane was observed when incubated with 1 mM glucose compared to 25 mM glucose. The addition of azas erin or deprivation of glutamine at 25 mM glucose did not increase the gluc ose transport activity to the level obtained with 1 mM glucose. PD98059 did not affect glucose transport activity when incubated with 1 mM or 25 mM gl ucose. In conclusion, the present study is the first to show that, in 3T3-L 1 adipocytes, chronic exposure to low (1 mM) and high (25 mM) glucose leads to different insulin-stimulated glucose transport activities. These differ ences result from the difference in the expression and plasma membrane dist ribution of GLUT1, but not of GLUT4, and the hexosamine biosynthesis pathwa y or extracellular signal-regulated protein kinase is not involved.