1 Case Western Reserve University, Cleveland, OH.
2 Nutrition and Movement Sciences, Maastricht University, Maastricht, The Netherlands.
3 Integrated Physiology and Molecular Medicine Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA.
4 Human Bioenergetics Laboratory, University of Michigan, Ann Arbor, MI.
5 Department of Gastroenterology & Hepatology, Cleveland Clinic, Cleveland, OH.
PURPOSE: We aimed to determine the immediacy of exercise intervention on liver-specific metabolic processes in Non-alcoholic fatty liver disease (NAFLD).
METHODS: We undertook a short-term (7-day) exercise training study (60 min/day treadmill walking at 80-85% of maximum heart rate) in obese adults (N=13, 58±3 years, 34.3±1.1 kg/m, >5% hepatic lipid by H-MR spectroscopy). Insulin sensitivity (ISI) was estimated by oral glucose tolerance test using the Soonthorpun model. Hepatic insulin extraction (HIE) was calculated as the molar difference in AUC for insulin and C-peptide (HIE= 1-(AUCInsulin÷AUCC-Pep)).
RESULTS: The increase in HIE, VO2max and ISI following the intervention was 9.8%, 9.8% and 34%, respectively (all P<0.05). Basal fat oxidation increased (Pre: 47±6 Vs Post: 65±6 mg/min, P<0.05) and carbohydrate oxidation decreased (Pre: 160±20 Vs Post: 112±15 mg/min, P<0.05) with exercise training. After the intervention, HIE correlated positively with adiponectin (r=0.56, P<0.05) and negatively with TNF-α (r=-0.78, P<0.001).
CONCLUSIONS: By increasing hepatic insulin extraction along with peripheral insulin sensitivity, aerobic exercise training rapidly reverses some of the underlying physiological mechanisms associated with NAFLD, in a weight-loss independent manner. This reversal could potentially act through adipokine-related pathways.