Abstract
BackgroundNon-alcoholic fatty liver disease (NAFLD) is rapidly turning into the most common liver disorder worldwide. One of the strategies that has been shown to effectively improve NAFLD is regular exercise, which seems to lower steatosis partly independent of weight loss. However, limited data are available about the mechanisms involved. The aim of the present study was to identify the mechanisms underlying the effect of regular exercise on liver steatosis.MethodsNon-obese male mice were rendered steatotic by feeding a sucrose-enriched choline-deficient diet. They were then subjected to daily treadmill running for three weeks, whereas the control mice remained sedentary.ResultsCompared to the untrained mice, trained mice showed similar adipose tissue mass but had significantly reduced size of lipid droplets in the liver coupled with a reduction in liver triglyceride content (~30 %, P < 0.05). Levels of various plasma lipid parameters and plasma glucose were similar between the trained and untrained mice, whereas levels of hepatic glycogen were significantly higher in the trained mice. Hepatic triglyceride secretion rate and de novo lipogenesis were unchanged between the two sets of mice, as were indicators of lipolysis and autophagy. Finally, whole genome expression profiling indicated a mild stimulatory effect of exercise training on PPARα-mediated regulation of oxidative metabolism, including fatty acid oxidation.ConclusionsTaken together, our study suggests that the lowering of hepatic steatosis by repeated exercise is likely due to activation of fuel oxidation pathways in liver.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is rapidly turning into the most common liver disorder worldwide
The non-obese steatosis model consisted of five weeks of feeding C57BL/6 mice a diet enriched in sucrose but deficient in choline
Gene expression analysis by qPCR showed significant upregulation of a limited number of genes involved in hepatic lipogenesis, including stearoylCoA desaturase (Scd1), fatty acid synthase (Fasn) and Glycerol 3-phosphate acyltransferase (Gpam) in the mice fed sucrose-enriched choline-deficient diet (SECDD) (Fig. 1d)
Summary
Non-alcoholic fatty liver disease (NAFLD) is rapidly turning into the most common liver disorder worldwide. One of the strategies that has been shown to effectively improve NAFLD is regular exercise, which seems to lower steatosis partly independent of weight loss. The aim of the present study was to identify the mechanisms underlying the effect of regular exercise on liver steatosis. Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver disorders worldwide. The main initial feature of NAFLD is hepatic steatosis, defined by hepatic lipid levels in excess of 5 % of liver weight, which can further progress to steatohepatitis, hepatic fibrosis and cirrhosis [2]. Excess storage of lipids in the liver can be caused by a number of metabolic derangements including defective fatty acid oxidation, enhanced lipogenesis, impaired triglyceride secretion and increased uptake of fatty acids from the circulation [3]. Evidence abounds that insulin resistance promotes a fatty liver, while at the same time a fatty liver may lead
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