Clinical Trials Study
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Sep 28, 2016; 8(27): 1137-1148
Published online Sep 28, 2016. doi: 10.4254/wjh.v8.i27.1137
Independent effects of diet and exercise training on fat oxidation in non-alcoholic fatty liver disease
Ilaria Croci, Nuala M Byrne, Veronique S Chachay, Andrew P Hills, Andrew D Clouston, Trisha M O’Moore-Sullivan, Johannes B Prins, Graeme A Macdonald, Ingrid J Hickman
Ilaria Croci, Veronique S Chachay, School of Human Movement and Nutrition Sciences, University of Queensland, St. Lucia 4072, Australia
Ilaria Croci, Veronique S Chachay, Ingrid J Hickman, Translational Research Institute, the University of Queensland Diamantina Institute, Woolloongabba 4102, Australia
Nuala M Byrne, Bond Institute of Health and Sport, Bond University, Robina 4229, Australia
Nuala M Byrne, Institute of Health and Biomedical Innovation, Queensland University of Technology, Kelvin Grove 4059, Australia
Andrew P Hills, School of Health Sciences, University of Tasmania, Launceston 7250, Australia
Andrew P Hills, Trisha M O’Moore-Sullivan, Johannes B Prins, Ingrid J Hickman, Mater Research Institute University of Queensland, Brisbane 4101, Australia
Andrew D Clouston, Graeme A Macdonald, School of Medicine, the University of Queensland, Brisbane 4102, Australia
Graeme A Macdonald, Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Woolloongabba 4102, Australia
Graeme A Macdonald, Translational Research Institute, Woolloongabba 4102, Australia
Ingrid J Hickman, Department of Nutrition and Dietetics, Princess Alexandra Hospital, Woolloongabba 4102, Australia
Author contributions: Croci I wrote the paper; Croci I, Byrne NM, Chachay VS, Hills AP, Clouston AD, O’Moore-Sullivan TM, Prins JB, Macdonald GA and Hickman IJ designed the research; Croci I, Chachay VS, O’Moore-Sullivan TM, Macdonald GA and Hickman IJ collected data; Croci I, Hickman IJ and Clouston AD analyzed the data; Hickman IJ obtained funding; all authors approved the manuscript.
Supported by The National Health and Medical Research Council of Australia; and the Lions Medical Research Foundation.
Institutional review board statement: The study was approved by the Human Research Ethics Committees of the Princess Alexandra Hospital and the University of Queensland.
Clinical trial registration statement: This registration policy applies to prospective, randomized, controlled trials only.
Informed consent statement: All study participants, or their legal guardian, provided informed written consent prior to study enrollment.
Conflict-of-interest statement: The authors have no conflicts of interest to disclose.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Ilaria Croci, PhD, School of Human Movement and Nutrition Sciences, University of Queensland, Blair Drive, St. Lucia 4072, Australia. ilaria.croci@uqconnect.edu.au
Telephone: +61-7-33656851 Fax: +61-7-33656877
Received: April 30, 2016
Peer-review started: May 3, 2016
First decision: June 17, 2016
Revised: July 21, 2016
Accepted: August 17, 2016
Article in press: August 18, 2016
Published online: September 28, 2016
Abstract
AIM

To investigate the independent effects of 6-mo of dietary energy restriction or exercise training on whole-body and hepatic fat oxidation of patients with non-alcoholic fatty liver disease (NAFLD).

METHODS

Participants were randomised into either circuit exercise training (EX; n = 13; 3 h/wk without changes in dietary habits), or dietary energy restriction (ER) without changes in structured physical activity (ER; n = 8). Respiratory quotient (RQ) and whole-body fat oxidation rates (Fatox) were determined by indirect calorimetry under basal, insulin-stimulated and exercise conditions. Severity of disease and steatosis was determined by liver histology; hepatic Fatox was estimated from plasma β-hydroxybutyrate concentrations; cardiorespiratory fitness was expressed as VO2peak. Complete-case analysis was performed (EX: n = 10; ER: n = 6).

RESULTS

Hepatic steatosis and NAFLD activity score decreased with ER but not with EX. β-hydroxybutyrate concentrations increased significantly in response to ER (0.08 ± 0.02 mmol/L vs 0.12 ± 0.04 mmol/L, P = 0.03) but remained unchanged in response to EX (0.10 ± 0.03 mmol/L vs 0.11 ± 0.07 mmol/L, P = 0.39). Basal RQ decreased (P = 0.05) in response to EX, while this change was not significant after ER (P = 0.38). VO2peak (P < 0.001) and maximal Fatox during aerobic exercise (P = 0.03) improved with EX but not with ER (P > 0.05). The increase in β-hydroxybutyrate concentrations was correlated with the reduction in hepatic steatosis (r = -0.56, P = 0.04).

CONCLUSION

ER and EX lead to specific benefits on fat metabolism of patients with NAFLD. Increased hepatic Fatox in response to ER could be one mechanism through which the ER group achieved reduction in steatosis.

Keywords: Non-alcoholic steatohepatitis, Steatosis, Fat and carbohydrate oxidation, Exercise, Fitness, Beta-hydroxybutyrate, Ketone bodies, Fatty acid oxidation

Core tip: We investigated hepatic fat oxidation and whole-body substrate oxidation under basal, insulin-stimulated and exercise conditions before and after 6 mo of circuit exercise training (EX) or dietary energy restriction (ER) in patients with non-alcoholic fatty liver disease. ER increased β-hydroxybutyrate concentrations (a marker of hepatic fat oxidation) and reduced severity of steatosis, but did not change substrate oxidation rates during acute exercise. EX improved substrate oxidation under basal, insulin-stimulated and exercise conditions, but not β-hydroxybutyrate concentrations and severity of disease. Increase in β-hydroxybutyrate was associated with decrease in hepatic steatosis and this could be one mechanism through which the ER group achieved reduction in steatosis.