Supachoke MangmoolTananat DenkaewWarisara ParichatikanondHitoshi KuroseMahidol UniversityKyushu University2018-12-212019-03-142018-12-212019-03-142017-01-01Biomolecules and Therapeutics. Vol.25, No.1 (2017), 44-5620054483197691482-s2.0-85008400398https://repository.li.mahidol.ac.th/handle/20.500.14594/42031© 2017 The Korean Society of Applied Pharmacology. Insulin resistance is characterized by the reduced ability of insulin to stimulate tissue uptake and disposal of glucose including cardiac muscle. These conditions accelerate the progression of heart failure and increase cardiovascular morbidity and mortality in patients with cardiovascular diseases. It is noteworthy that some conditions of insulin resistance are characterized by up-regulation of the sympathetic nervous system, resulting in enhanced stimulation of β-adrenergic receptor (βAR). Overstimulation of βARs leads to the development of heart failure and is associated with the pathogenesis of insulin resistance in the heart. However, pathological consequences of the cross-talk between the βAR and the insulin sensitivity and the mechanism by which βAR overstimulation promotes insulin resistance remain unclear. This review article examines the hypothesis that βARs overstimulation leads to induction of insulin resistance in the heart.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyArticleSCOPUS10.4062/biomolther.2016.128