Abstract

Lipids droplets (LD) are dynamics organelles that accumulate neutral lipids during nutrient surplus. LD alternates between periods of growth and consumption through regulated processes including as de novo lipogenesis, lipolysis and lipophagy. The liver is a central tissue in the regulation of lipid metabolism. Non-Alcoholic Fatty Liver Diseases (NAFLD) is result of the accumulation of LD in liver. Several works have been demonstrated a positive effect of exercise on reduction of liver fat. However, the study of the exercise on liver LD dynamics is far from being understood. Here we investigated the effect of chronic exercise in the regulation of LD dynamics using a mouse model of high fat diet-induced NAFLD. Mice were fed with a high-fat diet or control diet for 12 weeks; then groups were divided into chronic exercise or sedentary for additional 8 weeks. Our results showed that exercise reduced fasting glycaemia, insulin and triacylglycerides, also liver damage. However, exercise did not affect the intrahepatic triacylglycerides levels and the number of LD but reduced their size. In addition, exercise decreased the SREBP-1c levels, without changes in lipolysis, mitochondrial proteins or autophagy/lipophagy markers. Unexpectedly in the control mice, exercise increased the number of LD, also PLIN2, SREBP-1c, FAS, ATGL, HSL and MTTP levels. Our findings show that exercise rescues the liver damage in a model of NAFLD reducing the size of LD and normalizing protein markers of de novo lipogenesis and lipolysis. Moreover, exercise increases proteins associated to LD dynamics in the control mice.