Abstract
Sedentary behavior constitutes a pandemic health threat contributing to the pathophysiology of obesity and type 2 diabetes (T2D). Sedentarism is further associated with liver disease and particularly with nonalcoholic/metabolic dysfunction associated fatty liver disease (NAFLD/MAFLD). Insulin resistance (IR) represents an early pathophysiologic key element of NAFLD/MAFLD, prediabetes and T2D. Current treatment guidelines recommend regular physical activity. There is evidence, that physical exercise has impact on a variety of molecular pathways, such as AMP-activated protein kinase and insulin signaling as well as glucose transporter 4 translocation, modulating insulin action, cellular substrate flow and in particular ectopic lipid and glycogen storage in a positive manner. Therefore, physical exercise can lead to substantial clinical benefit in persons with diabetes and/or NAFLD/MAFLD. However, experience from long term observational studies shows that the patients’ motivation to exercise regularly appears to be a major limitation. Strategies to integrate everyday physical activity (i.e., nonexercise activity thermogenesis) in lifestyle treatment schedules might be a promising approach. This review aggregates evidence on the impact of regular physical activity on selected molecular mechanisms as well as clinical outcomes of patients suffering from IR and NAFLD/MAFLD.
Highlights
The term nonalcoholic fatty liver disease (NAFLD) was defined in the 1980s to describe exceeding hepatocellular triacylglycerol accumulation in absence of significant alcohol intake, viral and autoimmune liver disease [1]
The authors of this study suggest that skeletal muscle Insulin resistance (IR) and lipid accumulation are likely due to lifestyle factors rather than inherent ageing of skeletal muscle [76]
In support of the concept of metabolic flexibility it is believed that an adaptive response to regular physical training, allowing a larger contribution of the local lipid greater intramyocellular lipid (IMCL) storage capacity in athletes represents an adaptive response to regular pool as an energetic substrate source during exercise in order to preserve glycogen [89,91]
Summary
The term nonalcoholic fatty liver disease (NAFLD) was defined in the 1980s to describe exceeding hepatocellular triacylglycerol accumulation in absence of significant alcohol intake, viral and autoimmune liver disease [1]. The metabolic condition of skeletal muscle, the organ system most impacted by physical exercise, was recently found to be influenced by liver lipid status in a dose dependent fashion [46]. Guidelines on T2D management suggest regular physical activity as one causal treatment option [48,49] This treatment strategy could exert beneficial effects under conditions of NAFLD/MAFLD [50]. Current guidelines on the clinical management of metabolic fatty liver disease include such recommendations, evidence is sparse and potential underlying molecular mechanisms are fragmentarily understood [51]
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