Open AccessEffect of the Combination of Training and ERRα Inhibition on Liver Metabolism by Modulation of PDK4 and LXR-α Expression in STZ-Induced Diabetic and Healthy Rats
Author(s) -
Yaser MasoumiArdakani,
Soheil Aminizadeh,
Beydolah Shahouzehi
Publication year - 2020
Publication title -
biointerface research in applied chemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.216
H-Index - 11
ISSN - 2069-5837
DOI - 10.33263/briac106.70117022
Subject(s) - pdk4 , endocrinology , medicine , downregulation and upregulation , diabetes mellitus , streptozotocin , liver x receptor , endurance training , chemistry , transcription factor , nuclear receptor , biochemistry , gene
Diabetes is a public health problem that affects life quality. Exercise training (ET) and controlled dietary habits improve metabolic diseases such as diabetes. The mechanisms by which exercise training ameliorate metabolic diseases are not fully clear. We designed the current study to evaluate the combination of ERRα suppression and ET effects on the expression of LXR-α, PDK4, and PPARα in healthy and STZ-induced diabetic rats. Fifty-six male Wistar rats were divided into 8 groups (n = 7) as follows; control, diabetic control (a single dose of 45 mg/kg of STZ), ERRα inhibition group (received 0.48 mg/kg of XCT790), endurance training, diabetic rats which received XCT790, diabetic rats which performed endurance training, rats which received XCT790 and performed endurance training, and diabetic rats which received XCT790 and also performed endurance training. Expression of the target gene and protein was carried out on the liver tissue. Our results showed that ET significantly increased PDK4, PPARα, and ERRα expression. ERRα suppression significantly increased LXR-α and PDK4 expression in healthy rats compared to the healthy control group. In the diabetic group with ERRα suppression, LXR-α expression significantly upregulated. The combination of ET and ERRα suppression did not change LXR-α expression compared to healthy and diabetic groups (CTL/ERR), but the expression of PDK4, PPARα, and ERRα was significantly upregulated.