Prolonged stimulation of β 2 -adrenergic receptor with β 2 -agonists impairs insulin actions in H9c2 cells
Insulin resistance is a condition in which there is a defect in insulin actions to induce glucose uptake into the cells. Overstimulation of β -adrenergic receptors (β ARs) is associated with the pathogenesis of insulin resistance in the heart. However, the mechanisms by which β -agonists affect insu...
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Published in | Journal of pharmacological sciences Vol. 138; no. 3; p. 184 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Japan
01.11.2018
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Subjects | |
Online Access | Get full text |
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Summary: | Insulin resistance is a condition in which there is a defect in insulin actions to induce glucose uptake into the cells. Overstimulation of β
-adrenergic receptors (β
ARs) is associated with the pathogenesis of insulin resistance in the heart. However, the mechanisms by which β
-agonists affect insulin resistance in the heart are incompletely understood. The β
-agonists are used for treatment of asthma due to bronchodilating effects. We also investigated the effects of β
-agonists in human bronchial smooth muscle (HBSM) cells. In this study, we demonstrate that chronic treatment with salbutamol, salmeterol, and formoterol inhibited insulin-induced glucose uptake and GLUT4 synthesis in H9c2 myoblast cells. Sustained β
AR stimulation also attenuated GLUT4 translocation to the plasma membrane, whereas short-term stimulation had no effect. In HBSM cells, prolonged treatment with β
-agonists had no effect on insulin-induced glucose uptake and did not alter insulin-induced expressions of GLUT1, GLUT4, and GLUT10. In addition, genetic polymorphisms at amino acid positions 16 and 27 of β
AR are linked to insulin resistance by significant suppression of GLUT4 translocation compared to wild-type. Thus, prolonged β
AR stimulation by β
-agonists impairs insulin actions through suppression of GLUT synthesis and translocation only in H9c2 cells. |
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ISSN: | 1347-8648 |