Skip to main content
Log in

The adaptations induced by Estrogen Related Receptor alpha (ERRα) disruption and exercise training on healthy and diabetic rat’s liver

  • Original Article
  • Published:
Biologia Aims and scope Submit manuscript

Abstract

Diabetes is a widespread metabolic disorder that needs specific management and researchers focused on exercise training and pharmacological interventions for diabetes management. Endurance training (ET) and ERRα gained attention as a potential therapeutic target for diabetes management. We investigated ET and ERRα inhibition effects on the expression of SIRT1 and AMPK in healthy and STZ-induced diabetic rats’ liver. Fifty-six Wistar rats were divided into 8 groups as follows (n = 7); group 1, control with no treatment; group 2, diabetic control group that received a single dose of STZ; group 3, ERRα inhibited group that received XCT 790; group 4, endurance training (ET); group 5, diabetic rats with ERRα inhibition; group 6, diabetic rats that performed ET; group 7, ERRα inhibition and ET; and group 8, diabetic rats with ERRα inhibition and performed ET. After 4 weeks, the animals were sacrificed and the liver was used for Real-Time PCR and Western blotting. Our results showed that ET significantly increased AMPK and SIRT1 gene and protein, and ERRα gene expression in healthy and diabetic rats compared to healthy and diabetic control groups. ERRα inhibition increased AMPK, SIRT1, SREBP-1c and ACC expression compared to control and ET groups. In healthy and diabetic rats, the combination of ERRα inhibition and ET significantly increased AMPK, SIRT1, SREBP-1c and ACC expression compared to healthy and diabetic control animals. Briefly, the combination of ET and ERRα disruption probably can be considered as a potential therapeutic intervention in diabetes but this hypothesis needs more evaluation to be cleared.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Fig. 1
Fig. 2
Fig. 3
Fig. 4
Fig. 5
Fig. 6
Fig. 7

Similar content being viewed by others

Abbreviations

ACC:

Acetyl CoA carboxylase

AMPK:

AMP-activated protein kinase

CPT1:

Carnitine palmitoyl transferase I

cDNA:

Complementary DNA

CTL:

Control

cAMP:

Cyclic adenosine monophosphate

ET:

Endurance training

ECL:

Enhanced Chemiluminescence

ERRα:

Estrogen related receptor alpha

FBG:

Fasting blood glucose

FA:

Fatty acid

FAO:

Fatty acid oxidation

FAS:

Fatty acid synthase

GPAT:

Glycerol-3-phosphate acyltransferase

HGP:

Hepatic glucose production

HFD:

High-fat diet

IR:

Insulin resistance

LXRs:

Liver X Receptors

NEFA:

Non-esterified fatty acids

PPARγ:

Peroxisome proliferator-activated receptor γ

PGC-1α:

Peroxisome-proliferated activated receptor coactivator-1 α

p-ACC:

phosphorylated ACC

PVDF:

Polyvinylidene Difluoride

PKC:

Protein kinase C

SDS-PAGE:

Sodium dodecyl sulfate polyacrylamide gel electrophoresis

SIRT1:

Sirtuin 1

SCD1:

Stearoyl-CoA desaturase-1

SREBP-1c:

Sterol regulatory element-binding proteins-1c

TBS-T:

Tris-buffered saline and Tween 20

References

Download references

Acknowledgements

The present article was financially supported by the Kerman University of Medical Sciences, Kerman, Iran.

Funding

This study was supported and funded by Kerman Medical University Research Council (grant number 95000199).

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Beydolah Shahouzehi.

Ethics declarations

Conflict of interest

The authors declare that they have no conflict of interest.

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Masoumi-Ardakani, Y., Aminizadeh, S. & Shahouzehi, B. The adaptations induced by Estrogen Related Receptor alpha (ERRα) disruption and exercise training on healthy and diabetic rat’s liver. Biologia 75, 2341–2350 (2020). https://doi.org/10.2478/s11756-020-00532-9

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.2478/s11756-020-00532-9

Keywords

Navigation