Open AccessHepatic Knockdown of Endothelin Type A Receptor (ETAR) Ameliorates Hepatic Insulin Resistance and Hyperglycemia Through Suppressing p66Shc-Mediated Mitochondrial Fragmentation in High-Fat Diet-Fed Mice
Author(s) -
Feng Li,
Songhua Wang,
Feng Chen,
Cheng Zhang,
Qiao Wang,
Yuting Zhao,
Zifeng Zhang
Publication year - 2021
Publication title -
diabetes, metabolic syndrome and obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.853
H-Index - 43
ISSN - 1178-7007
DOI - 10.2147/dmso.s299570
Subject(s) - gene knockdown , insulin resistance , medicine , endocrinology , biology , insulin receptor , receptor , insulin , apoptosis , biochemistry
Emerging evidence from animal studies and clinical trials indicates that systemic inhibition of endothelin1 (ET1) signaling by endothelin receptor antagonists improves pathological features of diabetes and its complications. It is indicated that endothelin type A receptor (ETAR) plays a major role in ET1-mediated pathophysiological actions including diabetic pathology. However, the effects as well as the mechanistic targets of hepatic ET1/ETAR signaling inhibition on the pathology of metabolic diseases remain unclear. This study aimed to investigate the beneficial effects as well as the underlying mechanisms of hepatic ETAR knockdown on metabolism abnormalities in high-fat diet (HFD)-fed mice.