Key result
Exercise regulates hepatokines, including FGF21, fetuin-A, ANGPTL4, and follistatin, which serve as molecular transducers of its metabolic benefits in chronic diseases.
Why the study?
Hepatocytes secrete hepatokines in response to physical activity that regulate metabolic homeostasis, highlighting the emerging endocrine role of the liver.
Does exercise regulate hepatokines to mediate metabolic benefits in chronic metabolic diseases?
Does exercise regulate hepatokines to mediate metabolic benefits in chronic metabolic diseases?
This review highlights the role of hepatokines as molecular transducers that mediate the systemic metabolic benefits of exercise in chronic diseases.
May inform hepatokine-targeted therapies; leaves open validation in prospective trials.
Exercise has health benefits and prevents a range of chronic diseases caused by physiological and biological changes in the whole body. Generally, the metabolic regulation of skeletal muscle through exercise is known to have a protective effect on the pathogenesis of metabolic syndrome, non-alcoholic fatty liver disease (NAFLD), type 2 diabetes (T2D), and cardiovascular disease (CVD). Besides this, the importance of the liver as an endocrine organ is a hot research topic. Hepatocytes also secrete many hepatokines in response to nutritional conditions and/or physical activity. In particular, certain hepatokines play a major role in the regulation of whole-body metabolic homeostasis. In this review, we summarize the recent research findings on the exercise-mediated regulation of hepatokines, including fibroblast growth factor 21, fetuin-A, angiopoietin-like protein 4, and follistatin. These hepatokines serve as molecular transducers of the metabolic benefits of physical activity in chronic metabolic diseases, including NAFLD, T2D, and CVDs, in various tissues.
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Seo et al. (2021) conducted a review in Metabolic syndrome, non-alcoholic fatty liver disease, type 2 diabetes, and cardiovascular disease. Exercise was evaluated. Exercise regulates hepatokines, including FGF21, fetuin-A, ANGPTL4, and follistatin, which serve as molecular transducers of its metabolic benefits in chronic diseases.
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