4.7 Article

Exercise Combats Hepatic Steatosis: Potential Mechanisms and Clinical Implications

Journal

DIABETES
Volume 69, Issue 4, Pages 517-524

Publisher

AMER DIABETES ASSOC
DOI: 10.2337/dbi18-0043

Keywords

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Funding

  1. Veterans Affairs (VA) Merit Grant [I01BX003271]
  2. National Institutes of Health (NIH) [R01 DK113701]
  3. VA Merit Grant [1I01BX002567]
  4. NIH [R01 KD121497, R01 AR071263]

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Hepatic steatosis, the excess storage of intrahepatic lipids, is a rampant clinical problem associated with the obesity epidemic. Hepatic steatosis is linked to increased risk for insulin resistance, type 2 diabetes, and cardiovascular and advanced liver disease. Accumulating evidence shows that physical activity, exercise, and aerobic capacity have profound effects on regulating intrahepatic lipids and mediating susceptibility for hepatic steatosis. Moreover, exercise can effectively reduce hepatic steatosis independent of changes in body mass. In this perspective, we highlight 1) the relationship between obesity and metabolic pathways putatively driving hepatic steatosis compared with changes induced by exercise; 2) the impact of physical activity, exercise, and aerobic capacity compared with caloric restriction on regulating intrahepatic lipids and steatosis risk; 3) the effects of exercise training (modalities, volume, intensity) for treatment of hepatic steatosis, and 4) evidence for a sustained protection against steatosis induced by exercise. Overall, evidence clearly indicates that exercise powerfully regulates intrahepatic storage of fat and risk for steatosis.

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