Prolonged stimulation of β 2 -adrenergic receptor with β 2 -agonists impairs insulin actions in H9c2 cells

• Published in: Journal of pharmacological sciences Vol. 138; no. 3; p. 184
• Main Authors: Parichatikanond, Warisara, Nishimura, Akiyuki, Nishida, Motohiro, Mangmool, Supachoke
• Format: Journal Article
• Language: English
• Published: Japan 01.11.2018
• Subjects: Adrenergic beta-2 Receptor Agonists - pharmacology; Albuterol - pharmacology; Cells, Cultured; Formoterol Fumarate - pharmacology; Glucose - metabolism; Glucose Transport Proteins, Facilitative - biosynthesis; Glucose Transporter Type 1 - biosynthesis; Glucose Transporter Type 4 - biosynthesis; Humans; Insulin - pharmacology; Insulin Antagonists - pharmacology; Insulin Resistance; Polymorphism, Genetic; Receptors, Adrenergic, beta-2 - metabolism; Salmeterol Xinafoate - pharmacology; βAR polymorphism; Glucose uptake; β-Agonist; GLUT translocation; Insulin resistance

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...