Nitric oxide stimulates glucose transport through insulin-independent GLUT4 translocation in 3T3-L1 adipocytes
T Tanaka, K Nakatani, K Morioka… - European journal of …, 2003 - academic.oup.com
T Tanaka, K Nakatani, K Morioka, H Urakawa, N Maruyama, N Kitagawa, A Katsuki…
European journal of endocrinology, 2003•academic.oup.comObjective It is well known that nitric oxide synthase (NOS) is expressed and that it modulates
glucose transport in skeletal muscles. Recent studies have shown that adipose tIssues also
express inducible and endothelial nitric oxide synthase (eNOS). In the present study, we
investigated whether nitric oxide (NO) induces glucose uptake in adipocytes, and the
signaling pathway involved in the NO-stimulated glucose uptake in 3T3-L1 adipocytes.
Methods First, we determined the expression of eNOS in 3T3-L1 adipocytes, and then these …
glucose transport in skeletal muscles. Recent studies have shown that adipose tIssues also
express inducible and endothelial nitric oxide synthase (eNOS). In the present study, we
investigated whether nitric oxide (NO) induces glucose uptake in adipocytes, and the
signaling pathway involved in the NO-stimulated glucose uptake in 3T3-L1 adipocytes.
Methods First, we determined the expression of eNOS in 3T3-L1 adipocytes, and then these …
Objective
It is well known that nitric oxide synthase (NOS) is expressed and that it modulates glucose transport in skeletal muscles. Recent studies have shown that adipose tIssues also express inducible and endothelial nitric oxide synthase (eNOS). In the present study, we investigated whether nitric oxide (NO) induces glucose uptake in adipocytes, and the signaling pathway involved in the NO-stimulated glucose uptake in 3T3-L1 adipocytes.
Methods
First, we determined the expression of eNOS in 3T3-L1 adipocytes, and then these cells were treated with the NO donor sodium nitroprusside (SNP) and/or insulin, and glucose uptake and phosphorylation of insulin receptor substrate (IRS)-1 and Akt were evaluated. Moreover, we examined the effects of a NO scavenger, a guanylate cyclase inhibitor or dexamethasone on SNP-stimulated glucose uptake and GLUT4 translocation.
Results
SNP at a concentration of 50 mmol/l increased 2-deoxyglucose uptake (1.8-fold) without phosphorylation of IRS-1 and Akt. Treatment with the NO scavenger or guanylate cyclase inhibitor decreased SNP-stimulated glucose uptake to the basal level. Dexamethasone reduced both insulin- and SNP-stimulated glucose uptake with impairment of GLUT4 translocation.
Conclusion
NO is capable of stimulating glucose transport through GLUT4 translocation in 3T3-L1 adipocytes, via a mechanism different from the insulin signaling pathway.
Oxford University Press