Esaxerenone, a selective mineralocorticoid receptor blocker, improves insulin sensitivity in mice consuming high-fat diet

Esaxerenone is a novel, non-steroidal selective mineralocorticoid receptor (MR) blocker. MR activation plays a crucial role in the development of cardiovascular and metabolic diseases. In this study, we investigated the effects of esaxerenone on various metabolic parameters in mice. Esaxerenone (3 m...

Full description

Saved in:
Bibliographic Details
Published in:European journal of pharmacology 2022-09, Vol.931, p.175190-175190, Article 175190
Main Authors: Bavuu, Oyunbileg, Fukuda, Daiju, Ganbaatar, Byambasuren, Matsuura, Tomomi, Ise, Takayuki, Kusunose, Kenya, Yamaguchi, Koji, Yagi, Shusuke, Yamada, Hirotsugu, Soeki, Takeshi, Wakatsuki, Tetsuzo, Sata, Masataka
Format: Article
Language:English
Subjects:
Aldosterone
Esaxerenone
Insulin resistance
Insulin signaling
Mineralocorticoid receptor
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Esaxerenone is a novel, non-steroidal selective mineralocorticoid receptor (MR) blocker. MR activation plays a crucial role in the development of cardiovascular and metabolic diseases. In this study, we investigated the effects of esaxerenone on various metabolic parameters in mice. Esaxerenone (3 mg/kg/day) was orally administered to high-fat diet (HFD)-fed male C57BL/6 mice. Mice fed a normal diet (ND) served as controls. Glucose and insulin tolerance, plasma lipid levels, and transaminase levels were assessed as metabolic parameters. Macrophage accumulation in the adipose tissue was evaluated using histological analysis. 3T3-L1 adipocytes, HepG2 cells, and C2C12 myotubes were used for in vitro experiments. Gene expression and insulin signaling were examined using quantitative RT-PCR and western blotting, respectively. HFD successfully induced insulin resistance compared with that in ND. Esaxerenone ameliorated insulin resistance (P 
ISSN:0014-2999
1879-0712
DOI:10.1016/j.ejphar.2022.175190