J. Biochem, 1997, Vol. 122, No. 1 90-95
© 1997 Japanese Biochemical Society
research-article |
The ß3 -Adrenergic Agonist BRL37344 Increases Glucose Transport into L6 Myocytes through a Mechanism Different from That of Insulin1
Department of Medical Biochemistry, Ehime University School of Medicine Shigenobu, Ehime 791-02
3To whom correspondence should be addressed. E-mail: tshimazu{at}m.ehime-u.ac.jp
In the present study, we examined the effects of BRL37344, a selective ß3-adrenergic agonist, on glucose transport into L6 myocytes and the results were compared with the effects of insulin. Insulin increased 2-deoxyglucose (2-DG) uptake in a dose-dependent manner, with maximal stimulation at 10–7 M. BRL37344 ranging from 10–7 to 10–5 M also enhanced 2-DG uptake in the absence of insulin. The effects of insulin and BRL37344 were completely additive, suggesting that these two agents enhance glucose uptake by L6 myocytes through different mechanisms. In fact, BRL37344 apparently did not increase tyrosine phosphorylation of cellular proteins in L6 myocytes, whereas insulin stimulated tyrosine phosphorylation of 180–190 and 95 kDa proteins. Furthermore, BRL37344-induced increase in glucose transport was not blocked by wortmannin, an inhibitor of phos-phatidylinositol 3-kinase, whereas the insulin-induced effect was completely abolished. When L6 myocytes were incubated with insulin, the content of GLUT4 in the plasma membrane was increased. However, BRL37344 did not affect the GLUT4 content in the plasma membrane. BRL37344. did not increase the Vmax value for glucose uptake but decreased the Km, value, although insulin increased the Vmax value. These results suggest that BRL 37344 enhances glucose transport into L6 myocytes through a signaling pathway different from that of insulin and that the mechanism does not involve the translocation of GLUT4, but may be due to an increase in the intrinsic activity of GLUT present in the plasma membrane.
1This work was supported by grants from The Mitsubishi Foundation, the Uehara Memorial Foundation, the Japan Diabetes Foundation and Senri Life Science Foundation, and by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science, Sports and Culture of Japan.
2Present address: Department of Veterinary Physiology, Faculty of Agriculture, Gifu University, Gifu 501-11.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  K. Yea, J. Kim, J. H. Yoon, T. Kwon, J. H. Kim, B. D. Lee, H.-J. Lee, S. J. Lee, J.-I. Kim, T. G. Lee, et al. Lysophosphatidylcholine Activates Adipocyte Glucose Uptake and Lowers Blood Glucose Levels in Murine Models of Diabetes J. Biol. Chem., December 4, 2009; 284(49): 33833 - 33840. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. S. Hutchinson and T. Bengtsson AMP-Activated Protein Kinase Activation by Adrenoceptors in L6 Skeletal Muscle Cells: Mediation by {alpha}1-Adrenoceptors Causing Glucose Uptake Diabetes, March 1, 2006; 55(3): 682 - 690. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. H. Mulder, C. J. Tack, A. J. Olthaar, P. Smits, F. C. G. J. Sweep, and R. R. Bosch Adrenergic receptor stimulation attenuates insulin-stimulated glucose uptake in 3T3-L1 adipocytes by inhibiting GLUT4 translocation Am J Physiol Endocrinol Metab, October 1, 2005; 289(4): E627 - E633. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Chernogubova, D. S. Hutchinson, J. Nedergaard, and T. Bengtsson {alpha}1- and {beta}1-Adrenoceptor Signaling Fully Compensates for {beta}3-Adrenoceptor Deficiency in Brown Adipocyte Norepinephrine-Stimulated Glucose Uptake Endocrinology, May 1, 2005; 146(5): 2271 - 2284. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. S. Hutchinson and T. Bengtsson {alpha}1A-Adrenoceptors Activate Glucose Uptake in L6 Muscle Cells through a Phospholipase C-, Phosphatidylinositol-3 Kinase-, and Atypical Protein Kinase C-Dependent Pathway Endocrinology, February 1, 2005; 146(2): 901 - 912. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Chernogubova, B. Cannon, and T. Bengtsson Norepinephrine Increases Glucose Transport in Brown Adipocytes via {beta}3-Adrenoceptors through a cAMP, PKA, and PI3-Kinase-Dependent Pathway Stimulating Conventional and Novel PKCs Endocrinology, January 1, 2004; 145(1): 269 - 280. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Kanzaki, R. T. Watson, N. O. Artemyev, and J. E. Pessin The Trimeric GTP-binding Protein (Gq/G11) alpha Subunit Is Required for Insulin-stimulated GLUT4 Translocation in 3T3L1 Adipocytes J. Biol. Chem., March 15, 2000; 275(10): 7167 - 7175. [Abstract] [Full Text] [PDF]
|
|