TY - JOUR
T1 - β-Adrenergic receptor and insulin resistance in the heart
AU - Mangmool, Supachoke
AU - Denkaew, Tananat
AU - Parichatikanond, Warisara
AU - Kurose, Hitoshi
N1 - Funding Information:
This work was supported by National Science and Technology Development Agency (NSTDA) grant P-12-01409 and the Center of Excellence for Innovation in Drug Design and Discovery, Faculty of Pharmacy, Mahidol University to S. Mangmool, and by JSPS KAKENHI (25253011) and the Uehara Memorial Foundation to H. Kurose.
Publisher Copyright:
© 2017 The Korean Society of Applied Pharmacology.
PY - 2017/1
Y1 - 2017/1
N2 - 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.
AB - 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.
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U2 - 10.4062/biomolther.2016.128
DO - 10.4062/biomolther.2016.128
M3 - Article
AN - SCOPUS:85008400398
SN - 1976-9148
VL - 25
SP - 44
EP - 56
JO - Biomolecules and Therapeutics
JF - Biomolecules and Therapeutics
IS - 1
ER -
