HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Role of physical exercise on hepatic insulin, glucocorticoid and inflammatory signaling pathways in an animal model of non-alcoholic steatohepatitis.

AbstractAIMS:
Pro-inflammatory mediators, glucocorticoids and transforming growth factor (TGF)-β are implicated in the pathogenesis of non-alcoholic steatohepatitis (NASH)-related insulin resistance. As physical activity is beneficial against NASH, we analyzed the voluntary physical activity (VPA) and endurance training (ET) (preventive and therapeutic strategies) effects on hepatic insulin, pro-inflammatory and glucocorticoid signaling regulators/mediators in high-fat (Lieber-DeCarli) diet (HFD)-induced NASH.
MAIN METHODS:
Adult male Sprague-Dawley rats were divided in standard diet (SD) or HFD, with sedentary, VPA and ET animals in both diet regimens. Plasma glucose and insulin concentrations were analyzed; plasma insulin sensitivity index (ISI) was calculated. Hepatic insulin, pro-inflammatory and glucocorticoid signaling regulators/mediators were evaluated by Western blot or reverse transcriptase-PCR.
KEY FINDINGS:
ET improved ISI in both diet regimens. HFD-feeding increased interleukin-1β and induced a similar pattern on interleukin-6 and TGF-β, which were globally reduced by physical exercise. ET decreased HFD leukemia inhibitory factor level, SD+VPA animals presenting higher values than HFD+VPA animals. HFD increased the ratio of IRS-1(Ser307)/total IRS-1, which was completely mitigated by physical exercise. Physical exercise reduced total ERK and JNK (total and activated) expression in HFD. In SD vs. HFD, VPA presented higher activated JNK and ET presented higher total JNK. Generally, in HFD, the ratio (activated/total) of AKT, and each separately, decreased with exercise and also for activated AKT in SD. Overall, in both diets, exercise reduced 11β-hydroxysteroid dehydrogenase type 1. ET increased glucocorticoid receptor and reduced PTP1B in HFD.
SIGNIFICANCE:
Physical exercise mitigates the expression of pro-inflammatory mediators and positively modulates insulin and glucocorticoid signaling in NASH.
AuthorsE Passos, C D Pereira, I O Gonçalves, S Rocha-Rodrigues, N Silva, J T Guimarães, D Neves, A Ascensão, J Magalhães, M J Martins
JournalLife sciences (Life Sci) Vol. 123 Pg. 51-60 (Feb 15 2015) ISSN: 1879-0631 [Electronic] Netherlands
PMID25534442 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2014 Elsevier Inc. All rights reserved.
Chemical References
  • DNA Primers
  • Glucocorticoids
  • Inflammation Mediators
  • Insulin
  • Transforming Growth Factor beta
Topics
  • Animals
  • Blotting, Western
  • DNA Primers (genetics)
  • Diet, High-Fat (adverse effects)
  • Glucocorticoids (metabolism)
  • Inflammation Mediators (metabolism)
  • Insulin (metabolism)
  • Insulin Resistance (physiology)
  • Male
  • Motor Activity (physiology)
  • Non-alcoholic Fatty Liver Disease (complications, etiology, physiopathology)
  • Physical Conditioning, Animal (physiology)
  • Physical Endurance (physiology)
  • Rats
  • Rats, Sprague-Dawley
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction (physiology)
  • Statistics, Nonparametric
  • Transforming Growth Factor beta (metabolism)

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: