Adipose tissue inflammation and metabolic syndrome. The proactive role of probiotics.

Eur J Nutr

Centro de Referencia para Lactobacilos (CERELA), CONICET, Chacabuco 145 (4000), Tucumán, Argentina.

Published: February 2019

Purpose: The first part of this review focuses on the role of cells and molecules of adipose tissue involved in metabolic syndrome-induced inflammation and in the maintenance of this pathology. In the second part of the review, the potential role of probiotics-modulating metabolic syndrome-related inflammatory components is summarized and discussed.

Methods: The search for the current scientific literature was carried out using ScienceDirect, PubMed, and Google Scholar search engines. The keywords used were: metabolic syndrome, obesity, insulin resistant, adipose tissue, adipose tissue inflammation, chronic low-grade inflammation, immune cells, adipokines, cytokines, probiotics, and gut microbiota.

Results And Conclusions: Chronic low-grade inflammation that characterized metabolic syndrome can contribute to the development of the metabolic dysfunctions involved in the pathogenesis of its comorbidities. Adipose tissue is a complex organ that performs metabolic and immune functions. During metabolic syndrome, an imbalance in the inflammatory components of adipose tissue (immune cells, cytokines, and adipocytokines), which shift from an anti-inflammatory to a pro-inflammatory profile, can provoke metabolic syndrome linked complications. Further knowledge concerning the immune function of adipose tissue may contribute to finding better alternatives for the treatment or prevention of such disorders. The control of inflammation could result in the management of many of the pathologies related to metabolic syndrome. Due to the strong evidence that gut microbiota composition plays a role modulating the body weight, adipose tissue, and the prevalence of a low-grade inflammatory status, probiotics emerge as valuable tools for the prevention of metabolic syndrome and health recovery.

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Source
http://dx.doi.org/10.1007/s00394-018-1790-2DOI Listing

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