β-Adrenergic Receptor and Insulin Resistance in the Heart.
10.4062/biomolther.2016.128
- Author:
Supachoke MANGMOOL
1
;
Tananat DENKAEW
;
Warisara PARICHATIKANOND
;
Hitoshi KUROSE
Author Information
1. Department of Pharmacology, Faculty of Pharmacy, Mahidol University, Bangkok 10400, Thailand.
- Publication Type:Review
- Keywords:
β-adrenergic receptor;
β-blockers;
G protein-coupled receptor kinase;
Heart diseases;
Insulin resistance;
Protein kinase A
- MeSH:
Cardiovascular Diseases;
Cyclic AMP-Dependent Protein Kinases;
Glucose;
Heart Diseases;
Heart Failure;
Heart*;
Humans;
Insulin Resistance*;
Insulin*;
Mortality;
Myocardium;
Sympathetic Nervous System;
Up-Regulation
- From:Biomolecules & Therapeutics
2017;25(1):44-56
- CountryRepublic of Korea
- Language:English
-
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 β-adrenergic receptor (βAR). Over-stimulation 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 over-stimulation promotes insulin resistance remain unclear. This review article examines the hypothesis that βARs over-stimulation leads to induction of insulin resistance in the heart.
