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1 Third Department of Internal Medicine, Kyorin University, Mitaka, Tokyo, Japan
2 Department of Biochemistry, Kyorin University, Mitaka, Tokyo, Japan
* To whom correspondence should be addressed. E-mail: ishida{at}kyorin-u.ac.jp.
To determine whether the increase in glucose uptake following AMP-activated protein kinase (AMPK) activation in adipocytes is mediated by accelerated GLUT4 translocation into plasma membrane, we constructed a chimera between GLUT4 and enhanced green fluorescent protein (GLUT4-eGFP), and transferred its cDNA into the nucleus of 3T3-L1 adipocytes. Then, the dynamics of GLUT4-eGFP translocation was visualized in living cells using laser scanning confocal microscopy. It was revealed that the stimulation with 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) and 2, 4-dinitrophenol (DNP), known activators of AMPK, promptly accelerates its translocation within 4 min, as was found in the case of insulin stimulation. The insulin-induced GLUT4 translocation was markedly inhibited after the addition of wortmannin (p<0.01). However, the GLUT4 translocation through AMPK activators AICAR and DNP was not affected by wortmannin. Insulin- and AMPK-activated translocation of GLUT4 was not inhibited by SB203580, an inhibitor of p38 mitogen-activated protein kinase (MAPK). The glucose uptake was significantly increased after the addition of AMPK activators AICAR and DNP (p<0.05). The AMPK- and insulin-stimulated glucose uptake were similarly suppressed by wortmannin (p<0.05~0.01). In addition, SB203580 also significantly prevented the enhancement of glucose uptake induced by AMPK and insulin (p<0.05). These results suggest that AMPK-activated GLUT4 translocation in 3T3L1 adipocytes is mediated through insulin signaling pathway distal to the site of activated phosphatidylinositol 3-kinase, or through signaling system distinct from that activated by insulin. On the other hand, the increase of glucose uptake dependent on AMPK activators AICAR and DNP would be additionally due to enhancement of the intrinsic activity in translocated GLUT4 protein, possibly through p38 MAPK-dependent mechanism.
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