Adipose Tissue Dysfunction and the Therapeutic Role of Exercise

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 4754

Special Issue Editor


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Guest Editor
Department of Biomolecular Science, Università degli Studi di Urbino, 61029 Urbino, Italy
Interests: physical activity; brown adipose tissue; leptin; adipocytes; fat; white adipose tissue; obesity

Special Issue Information

Dear Colleagues,

Adipose tissue is a central metabolic organ in the regulation of whole-body energy homeostasis. Dysregulation in any one of the three primary functions of adipocytes (lipid storage, endocrine/paracrine function, and insulin responsiveness) can have major impacts on overall metabolic health. Moreover, adipose tissue dysfunction is a predictor of metabolic diseases and cardiovascular events, thus highlighting the relevance of research concerning the therapeutic strategies for the maintenance of "healthy adipose tissue".

Physical inactivity is a direct cause of the inflammation and metabolic dysfunction associated with obesity. Emerging evidence indicates that regular exercise could be the most important non-pharmacological strategy for the prevention and treatment of obesity and its related cardiovascular/metabolic diseases. The beneficial effects on the overall metabolic health (including improvements in glucose tolerance, insulin sensitivity, and the lowering of circulating lipid concentrations) have historically been attributed to adaptations in skeletal muscle. However, in recent years, there has been growing consensus for assigning exercise a therapeutic role to combat adipose tissue-derived metabolic dysfunction, even in the absence of weight loss.

In adipose tissue, exercise training reduces lipid content and inflammation, regulates browning and thermogenesis, and modulates the production of adipokines. However, the mechanisms by which exercise causes such adipose remodelling and whether or not the actions of exercise contribute to the systemic improvement of insulin sensitivity and metabolic health remain undefined.

Authors are encouraged to send their contributions, in the form of original manuscripts or reviews, that analyse the factors that trigger exercise-induced adipose adaptations and the underlying molecular mechanisms.

The aim of this Special Issue is to increase knowledge on the following:

  • the molecular and cellular biology and pathophysiology of adipose dysfunction.
  • the role of adipose tissue as a metabolically active, "exercise-responsive" organ, as well as elucidating a methodology for advanced exercise effectiveness.
  • exercise interventions that will specifically target adipose tissue metabolic health.
  • molecular signatures of exercise-induced adipose adaptations to achieve health-promoting therapies.

Dr. Rita De Matteis
Guest Editor

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Keywords

  • physical activity
  • exercise prescription
  • white adipose tissue
  • brown adipose tissue
  • browning
  • metabolic disease
  • hypertrophic adipocyte
  • oxidative stress
  • inflammation
  • immunometabolism
  • endoplasmic reticulum
  • adipokines
  • batokines

Published Papers (1 paper)

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Research

19 pages, 35906 KiB  
Article
Exercise Inhibits NLRP3 Inflammasome Activation in Obese Mice via the Anti-Inflammatory Effect of Meteorin-like
by Hafiz Muhammad Ahmad Javaid, Namood E Sahar, De-Li ZhuGe and Joo Young Huh
Cells 2021, 10(12), 3480; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10123480 - 9 Dec 2021
Cited by 31 | Viewed by 4198
Abstract
Obesity is associated with chronic low-grade inflammation. The benefits of exercise are partly attributed to its anti-inflammatory effect, but whether exercise can regulate NLRP3 inflammasome activation in obese adipose tissue remains unknown. Meteorin-like (METRNL), a recently discovered myokine, has been implicated in mediating [...] Read more.
Obesity is associated with chronic low-grade inflammation. The benefits of exercise are partly attributed to its anti-inflammatory effect, but whether exercise can regulate NLRP3 inflammasome activation in obese adipose tissue remains unknown. Meteorin-like (METRNL), a recently discovered myokine, has been implicated in mediating the effect of exercise on metabolism. Herein, we examined the effect of exercise and METRNL on NLRP3 inflammasome activation. High-fat diet (HFD)-induced obese mice were subjected to treadmill exercise for 8 weeks. A subgroup of HFD mice was switched to normal chow with the exercise intervention. Exercise and diet attenuated weight gain, fat accumulation, and insulin resistance in obese mice. In addition, exercise downregulated gene and protein levels of inflammasome markers, including NLRP3 and caspase-1, in adipose tissue. In isolated bone marrow-derived macrophages, activation of NLRP3 inflammasome was suppressed in the exercise group, as confirmed by the downregulation of IL-1β and IL-18. Exercise significantly enhanced the expression of METRNL in various muscle depots, and further in vitro analysis revealed that recombinant METRNL treatment inhibited IL-1β secretion in macrophages. In conclusion, exercise exerts its anti-inflammatory action by suppressing adipose tissue NLRP3 inflammasome, and this is, in part, associated with METRNL induction in muscle and its anti-inflammatory effects in macrophages. Full article
(This article belongs to the Special Issue Adipose Tissue Dysfunction and the Therapeutic Role of Exercise)
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