Exercise against nonalcoholic fatty liver disease: Possible role and mechanism of lipophagy.

Nonalcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease worldwide. NAFLD is prevalent in about 30% of people worldwide. The lack of physical activity is considered as one of the risks for NAFLD, and approximately one-third of NAFLD patients hardly engage in physical activity. It is acknowledged that exercise is one of the optimal non-pharmacological methods for preventing and treating NAFLD. Different forms of exercise such as aerobic exercise, resistance exercise and even simply physical activity in a higher level can be beneficial in reducing liver lipid accumulation and disease progression for NAFLD patients. In NAFLD patients, exercise is helpful in lowering steatosis and enhancing liver function. The mechanisms underlying the prevention and treatment of NAFLD by exercise are various and complex. Current studies on the mechanisms have focused on the pro-lipolytic, anti-inflammatory, and antioxidant and lipophagy. Promotion of lipophagy is regarded as an important mechanism for prevention and improvement of NAFLD by exercise. Recent studies have investigated the above mechanism, yet the potential mechanism has not been completely elucidated. Thus, in this review, we cover the recent advances of exercise-promoted lipophagy in NAFLD treatment and prevention. Furthermore, given the fact that exercise activates SIRT1, we discuss the possible regulatory mechanisms of lipophagy by SIRT1 during exercise. These mechanisms need to be verified by further experimental studies.

Moderate intensity treadmill exercise alters food preference via dopaminergic plasticity of ventral tegmental area-nucleus accumbens in obese mice.

Obesity has been associated with the excessive intake of palatable food as well as physical inactivity. To investigate the neurobiological mechanism underlying the exercised-induced prevention and treatment of obesity, the present study examined the effect of treadmill exercise on the preference for palatable food in mice. Levels of tyrosine hydroxylase (TH) in the ventral tegmental area-nucleus accumbens system were also analysed, as well as levels of dopamine, dopamine transporter, and D2 receptors in the nucleus accumbens. Forty C57BL/6J mice were randomly divided into a control group (CG, n=10) and a high-fat diet group (HG, N=30). Mice of the HG group were fed a high-fat diet for 12 weeks in order to induce a model of obesity, following which the obese mice were randomly divided into an obese control group (OG, n=11) and an obese+exercise group (OEG, n=12). OEG mice received 8 weeks of treadmill exercise intervention. Our results indicate that, relative to animals in the OG group, OEG mice exhibited significant decreases in the preference for high-fat diets and insulin resistance, along with increases in the preference for sucrose and milk, TH and D2 receptor expression, and levels of dopamine in the ventral tegmental area-nucleus accumbens system. These results suggest that moderate-intensity treadmill exercise can alter food preference in obese mice, which may be mediated by dopaminergic plasticity of the ventral tegmental area-nucleus accumbens and enhanced insulin sensitivity.