F Shojaee-Moradie1, D J Cuthbertson1, M Barrett1, N C Jackson1, R Herring1, E L Thomas1, J Bell1, G J Kemp1, J Wright1, A M Umpleby1. 1. Department of Diabetes and Metabolic Medicine (F.S.-M., M.B., N.C.J., A.M.U.), Faculty of Health and Medical Sciences, University of Surrey, Guildford GU2 7WG, United Kingdom; Metabolism and Nutrition Research Group (D.J.C., G.J.K.), Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool L69 7ZX, United Kingdom; Section of Investigative Medicine, Endocrinology, and Metabolism (E.L.T., J.B.), University of Westminster, London W1B2UW United Kingdom; and Centre for Diabetes, Endocrinology, and Research (R.H., J.W.), Royal Surrey County Hospital, Guildford GU2 7XX, United Kingdom.
Abstract
CONTEXT: Randomized controlled trials in nonalcoholic fatty liver disease (NAFLD) have shown that regular exercise, even without calorie restriction, reduces liver steatosis. A previous study has shown that 16 weeks of supervised exercise training in NAFLD did not affect total very low-density lipoprotein (VLDL) kinetics. OBJECTIVE: The objective of the study was to determine the effect of exercise training on intrahepatocellular fat (IHCL) and the kinetics of large triglyceride (TG)-rich VLDL1 and smaller denser VLDL2, which has a lower TG content. DESIGN: This was a 16-week randomized controlled trial. PATIENTS: A total of 27 sedentary patients with NAFLD participated in the trial. INTERVENTION: The intervention was composed of supervised exercise with moderate-intensity aerobic exercise or conventional lifestyle advice (control). MAIN OUTCOME: VLDL1 and VLDL2-TG and apolipoprotein B (apoB) kinetics were investigated using stable isotopes before and after the intervention. RESULTS: In the exercise group, maximal oxygen uptake increased by 31% ± 6% (mean ± SEM) and IHCL decreased from 19.6% (14.8%, 30.0%) to 8.9% (5.4%, 17.3%) (median [interquartile range]) with no significant change in maximal oxygen uptake or IHCL in the control group (change between groups, P < .001 and P = .02, respectively). Exercise training increased VLDL1-TG and apoB fractional catabolic rates, a measure of clearance, (change between groups, P = .02 and P = .01, respectively), and VLDL1-apoB production rate (change between groups, P = .006), with no change in VLDL1-TG production rate. Plasma TG did not change in either group. CONCLUSION: An increased clearance of VLDL1 may contribute to the significant decrease in liver fat after 16 weeks of exercise in NAFLD. A longer duration or higher-intensity exercise interventions may be needed to lower the plasma TG and VLDL production rate.
CONTEXT: Randomized controlled trials in nonalcoholic fatty liver disease (NAFLD) have shown that regular exercise, even without calorie restriction, reduces liver steatosis. A previous study has shown that 16 weeks of supervised exercise training in NAFLD did not affect total very low-density lipoprotein (VLDL) kinetics. OBJECTIVE: The objective of the study was to determine the effect of exercise training on intrahepatocellular fat (IHCL) and the kinetics of large triglyceride (TG)-rich VLDL1 and smaller denser VLDL2, which has a lower TG content. DESIGN: This was a 16-week randomized controlled trial. PATIENTS: A total of 27 sedentary patients with NAFLD participated in the trial. INTERVENTION: The intervention was composed of supervised exercise with moderate-intensity aerobic exercise or conventional lifestyle advice (control). MAIN OUTCOME: VLDL1 and VLDL2-TG and apolipoprotein B (apoB) kinetics were investigated using stable isotopes before and after the intervention. RESULTS: In the exercise group, maximal oxygen uptake increased by 31% ± 6% (mean ± SEM) and IHCL decreased from 19.6% (14.8%, 30.0%) to 8.9% (5.4%, 17.3%) (median [interquartile range]) with no significant change in maximal oxygen uptake or IHCL in the control group (change between groups, P < .001 and P = .02, respectively). Exercise training increased VLDL1-TG and apoB fractional catabolic rates, a measure of clearance, (change between groups, P = .02 and P = .01, respectively), and VLDL1-apoB production rate (change between groups, P = .006), with no change in VLDL1-TG production rate. Plasma TG did not change in either group. CONCLUSION: An increased clearance of VLDL1 may contribute to the significant decrease in liver fat after 16 weeks of exercise in NAFLD. A longer duration or higher-intensity exercise interventions may be needed to lower the plasma TG and VLDL production rate.
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