CCAAT/enhancer binding protein α maintains the ability of insulin-stimulated GLUT4 translocation in 3T3-C2 fibroblastic cells
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چکیده
منابع مشابه
Rab10 in insulin-stimulated GLUT4 translocation.
In fat and muscle cells, insulin stimulates the movement to and fusion of intracellular vesicles containing GLUT4 with the plasma membrane, a process referred to as GLUT4 translocation. Previous studies have indicated that Akt [also known as PKB (protein kinase B)] phosphorylation of AS160, a GAP (GTPase-activating protein) for Rabs, is required for GLUT4 translocation. The results suggest that...
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Activation of the sympathetic nervous system inhibits insulin-stimulated glucose uptake. However, the underlying mechanisms are incompletely understood. Therefore, we studied the effects of catecholamines on insulin-stimulated glucose uptake and insulin-stimulated translocation of GLUT4 to the plasma membrane in 3T3-L1 adipocytes. We found that epinephrine (1 microM) nearly halved insulin-stimu...
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Insulin increases muscle and fat cell glucose uptake by inducing the translocation of glucose transporter GLUT4 from intracellular compartments to the plasma membrane. Here, we have demonstrated that in 3T3-L1 adipocytes, DMSO at concentrations higher than 7.5% augmented cell surface GLUT4 levels in the absence and presence of insulin, but that at lower concentrations, DMSO only enhanced GLUT4 ...
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T2DM is primarily linked to obesity and insulin resistance—a decreased sensitivity of glucose response to normal insulin levels—which have been linked to defects in the insulin signaling pathway. Analysis of detailed mathematical models of insulin signaling should yield a better understanding of the underlying mechanisms of insulin resistance and its subsequent progression to T2DM. This may be ...
متن کاملInsulin-stimulated GLUT4 protein translocation in adipocytes requires the Rab10 guanine nucleotide exchange factor Dennd4C.
Insulin-stimulated translocation of the glucose transporter GLUT4 to the cell surface in fat and muscle cells is the basis for insulin-stimulated glucose transport. Studies in adipocytes strongly support the following molecular mechanism for this process. Insulin-elicited phosphorylation of the GTPase-activating protein TBC1D4 (AS160) suppresses its activity toward Rab10 and thereby leads to an...
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ژورنال
عنوان ژورنال: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
سال: 2005
ISSN: 0167-4889
DOI: 10.1016/j.bbamcr.2004.12.007