Nitric oxide stimulates glucose transport through insulin-independent GLUT4 translocation in 3T3-L1 adipocytes

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 (...

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Published in:European journal of endocrinology 2003-07, Vol.149 (1), p.61-67
Main Authors: TANAKA, Takashi, NAKATANI, Kaname, YANO, Yutaka, WADA, Hideo, NOBORI, Tsutomu, SUMIDA, Yasuhiro, ADACHI, Yukihiko, MORIOKA, Kohei, URAKAWA, Hideki, MARUYAMA, Noriko, KITAGAWA, Nagako, KATSUKI, Akira, ARAKI-SASAKI, Rika, HORI, Yasuko, GABAZZA, Esteban C
Format: Article
Language:English
Subjects:
3T3 Cells
Adipocytes - metabolism
Animals
Biological and medical sciences
Deoxyglucose - pharmacokinetics
Dexamethasone - pharmacology
Diabetes. Impaired glucose tolerance
Endocrine pancreas. Apud cells (diseases)
Endocrinology
Endocrinopathies
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Glucocorticoids - pharmacology
Glucose - pharmacokinetics
Glucose Transporter Type 4
Guanylate Cyclase - metabolism
Hypoglycemic Agents - pharmacology
Insulin - pharmacology
Insulin Receptor Substrate Proteins
Investigative techniques, diagnostic techniques (general aspects)
Medical sciences
Mice
Monosaccharide Transport Proteins - metabolism
Muscle Proteins
Nitric Oxide - metabolism
Nitric Oxide Donors - pharmacology
Nitric Oxide Synthase - genetics
Nitric Oxide Synthase Type II
Nitric Oxide Synthase Type III
Nitroprusside - pharmacology
Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques
Phosphoproteins - metabolism
Phosphorylation
Protein-Serine-Threonine Kinases
Proto-Oncogene Proteins - metabolism
Proto-Oncogene Proteins c-akt
RNA, Messenger - analysis
Signal Transduction - drug effects
Signal Transduction - physiology
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Summary: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. 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. 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. NO is capable of stimulating glucose transport through GLUT4 translocation in 3T3-L1 adipocytes, via a mechanism different from the insulin signaling pathway.
ISSN:0804-4643
1479-683X
DOI:10.1530/eje.0.1490061