Horm Metab Res 2013; 45(05): 359-363
DOI: 10.1055/s-0032-1331184
Original Basic
© Georg Thieme Verlag KG Stuttgart · New York

Mediation of AMP Kinase in the Increase of Glucose Uptake in L6 Cells Induced by Activation of Imidazoline I-2 Receptors

T.-T. Yang
1   Department of Pathology, School of Chinese Medicine for Post-Baccalaureate, I-Shou University, Kaohsiung City, Taiwan
,
P.-M. Ku
2   Department of Cardiology and Medical Research, Chi-Mei Medical Center, Yong Kang, Tainan City, Taiwan
,
C.-T. Hsu
3   Department of Pathology, Edah University Medical Center, Kaohsiung City, Taiwan
,
H.-H. Chung
4   Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan City, Taiwan
,
W.-J. Lee
5   Department of Emergency Medicine, Chi-Mei Medical Center, Yong Kang, Tainan City, Taiwan
,
J.-T. Cheng
2   Department of Cardiology and Medical Research, Chi-Mei Medical Center, Yong Kang, Tainan City, Taiwan
4   Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan City, Taiwan
6   Institute of Medical Science, College of Health Science, Chang Jung Christian University, Guei-Ren, Tainan City, Taiwan
› Author Affiliations
Further Information

Publication History

received 14 August 2012

accepted 05 November 2012

Publication Date:
07 December 2012 (online)

Abstract

Recent work using radioactive tracer indicates that activation of imidazoline I2 receptor (I2R) by guanidinium derivatives may increase the glucose uptake in the skeletal muscle. However, the effect of I2R activation on nonradioactive glucose uptake is still unknown. The ability of glucose uptake in cultured L6 cells is then determined using 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxyglucose (2-NBDG) as a fluorescence indicator. The changes in 5′-AMP-activated protein kinase (AMPK) expression were also identified by Western blot analysis. In the present study, 2-(2-benzofuranyl)-2-imidazoline (2-BFI) is used to stimulate I2R while 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR) is applied to activate AMPK directly. Both compounds can increase 2-NBDG in L6 cells in a concentration-dependent manner. Meanwhile, compound C at concentrations sufficient to inhibit AMPK blocked this increase of glucose uptake by 2-BFI or AICAR. However, only 2-BFI-induced glucose uptake action was dose-dependently blocked by BU224, a specific I2R antagonist, in L6 cells. Moreover, AMPK phosphorylation was markedly increased by 2-BFI or AICAR in L6 cells. Similarly, only the effect of 2-BFI was attenuated by BU224 in L6 cells. Thus, we suggest that AMPK is mediated in I2R activation for increase of glucose uptake in the skeletal muscle cell and I2R will be a new target for diabetic therapy.

 
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