Now showing items 1-4 of 4
Lipid mediators of insulin resistance: ceramide signalling down-regulates GLUT4 gene transcription in 3T3-L1 adipocytes.
(East Carolina University, 1996-10-01)
We have previously demonstrated that chronic exposure of 3T3- L1 adipocytes to tumour necrosis factor-α (TNF) resulted in a marked decrease (~90%) in cellular GLUT4 (insulin-responsive glucose transporter) mRNA content as ...
Ectopic expression of Hel-N1, an RNA-binding protein, increases glucose transporter (GLUT1) expression in 3T3-L1 adipocytes.
(East Carolina University, 1997-02)
3T3-L1 preadipocytes ectopically expressing the mammalian RNA-binding protein Hel-N1 expressed up to 10-fold more glucose transporter (GLUT1) protein and exhibited elevated rates of basal glucose uptake. Hel-N1 is a member ...
Insulin responsiveness in skeletal muscle is determined by glucose transporter (Glut4) protein level.
(East Carolina University, 1990-09-01)
Glucose transport in skeletal muscle is mediated by two distinct transporter isoforms, designated muscle/adipose glucose transporter (Glut4) and erythrocyte/HepG2/brain glucose transporter (Glutl), which differ in both ...
Tumour necrosis factor-alpha regulates expression of the CCAAT-enhancer-binding proteins (C/EBPs) alpha and beta and determines the occupation of the C/EBP site in the promoter of the insulin-responsive glucose-transporter gene in 3T3-L1 adipocytes.
(East Carolina University, 1999-03-15)
We have demonstrated previously that treatment of 3T3-L1 adipocytes with tumour necrosis factor-alpha (TNF) results in a rapid (4 h) and significant (75–80%) reduction in the rate of transcription of the GLUT4 gene. Control ...