Exercise Training Reduces Liver Fat and Increases Rates of VLDL Clearance But Not VLDL Production in NAFLD.

Abstract

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. 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. This was a 16-week randomized controlled trial. A total of 27 sedentary patients with NAFLD participated in the trial. The intervention was composed of supervised exercise with moderate-intensity aerobic exercise or conventional lifestyle advice (control). VLDL₁ and VLDL₂-TG and apolipoprotein B (apoB) kinetics were investigated using stable isotopes before and after the intervention. 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. 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.