Skeletal muscle adiponectin induction in obesity and exercise
Recent scientific efforts have focused on the detrimental effects that obesity has on the metabolic function of skeletal muscles and whether exercise can improve this dysfunction. In this regard, adiponectin, with important metabolic functions (e.g. insulin-sensitizer and anti-inflammatory), has bee...
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Veröffentlicht in: | Metabolism, clinical and experimental clinical and experimental, 2020-01, Vol.102, p.154008-154008, Article 154008 |
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Sprache: | eng |
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Zusammenfassung: | Recent scientific efforts have focused on the detrimental effects that obesity has on the metabolic function of skeletal muscles and whether exercise can improve this dysfunction. In this regard, adiponectin, with important metabolic functions (e.g. insulin-sensitizer and anti-inflammatory), has been recently described as a myokine that acts in an autocrine/paracrine manner. Earlier studies reported that muscle adiponectin could be induced by pro-inflammatory mediators (e.g. lipopolysaccharide), cytokines, and high-fat diets, providing a protective mechanism of this tissue against metabolic insults. However, when metabolic insults such as high-fat diets are sustained this protective response becomes dysregulated, making the skeletal muscle susceptible to metabolic impairments. Recent studies have suggested that exercise could prevent or even reverse this process. Considering that most scientific knowledge on adiponectin dysregulation in obesity is from the study of adipose tissue, the present review summarizes and discusses the literature available to date regarding the effects of obesity on skeletal muscle adiponectin induction, along with the potential effects of different exercise prescriptions on this response in an obesity context.
•Skeletal muscles produce adiponectin in an autocrine/paracrine manner.•Expression of muscle adiponectin isoforms are dysregulated in obesity.•Exercise restores adiponectin induction during high-fat feeding.•To date, no clinical studies are available on this topic. |
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ISSN: | 0026-0495 1532-8600 |
DOI: | 10.1016/j.metabol.2019.154008 |