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β-Adrenergic Receptor and Insulin Resistance in the Heart

  • Mangmool, Supachoke (Department of Pharmacology, Faculty of Pharmacy, Mahidol University) ;
  • Denkaew, Tananat (Department of Pharmacology, Faculty of Pharmacy, Mahidol University) ;
  • Parichatikanond, Warisara (Department of Pharmacology, Faculty of Pharmacy, Mahidol University) ;
  • Kurose, Hitoshi (Department of Pharmacology and Toxicology, Graduate School of Pharmaceutical Sciences, Kyushu University)
  • Received : 2016.06.16
  • Accepted : 2016.08.02
  • Published : 2017.01.01

Abstract

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 ${\beta}$-adrenergic receptor (${\beta}$AR). Overstimulation of ${\beta}$ARs 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 ${\beta}$AR and the insulin sensitivity and the mechanism by which ${\beta}$AR overstimulation promotes insulin resistance remain unclear. This review article examines the hypothesis that ${\beta}$ARs overstimulation leads to induction of insulin resistance in the heart.

Keywords

References

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