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Review
. 2016:2016:4036232.
doi: 10.1155/2016/4036232. Epub 2016 Sep 18.

Multiple Sclerosis and Obesity: Possible Roles of Adipokines

José de Jesús Guerrero-García  1 , Lucrecia Carrera-Quintanar  2 , Rocío Ivette López-Roa  3 , Ana Laura Márquez-Aguirre  4 , Argelia Esperanza Rojas-Mayorquín  5 , Daniel Ortuño-Sahagún  2
Affiliations
Review

Multiple Sclerosis and Obesity: Possible Roles of Adipokines

José de Jesús Guerrero-García et al. Mediators Inflamm. 2016.

Abstract

Multiple Sclerosis (MS) is an autoimmune disorder of the Central Nervous System that has been associated with several environmental factors, such as diet and obesity. The possible link between MS and obesity has become more interesting in recent years since the discovery of the remarkable properties of adipose tissue. Once MS is initiated, obesity can contribute to increased disease severity by negatively influencing disease progress and treatment response, but, also, obesity in early life is highly relevant as a susceptibility factor and causally related risk for late MS development. The aim of this review was to discuss recent evidence about the link between obesity, as a chronic inflammatory state, and the pathogenesis of MS as a chronic autoimmune and inflammatory disease. First, we describe the main cells involved in MS pathogenesis, both from neural tissue and from the immune system, and including a new participant, the adipocyte, focusing on their roles in MS. Second, we concentrate on the role of several adipokines that are able to participate in the mediation of the immune response in MS and on the possible cross talk between the latter. Finally, we explore recent therapy that involves the transplantation of adipocyte precursor cells for the treatment of MS.

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Conflict of interest statement

The authors declare that there is no conflict of interests regarding the publication of this article.

Figures

Figure 1
Figure 1
An integrative view of the possible involvement of some adipokines present in patients with multiple sclerosis (MS) at different disease stages. Obesity during adolescence constitutes a relevant risk factor for the later development of MS. Adult obesity negatively affects evolution of the disease and response to treatment in patients with MS. During relapsing-remitting stages, a decrease in adiponectin has been reported as well as, concomitantly, an increase in resistin, adipsin, and leptin concentrations (in serum or CSF or both). Additionally, A-FABP is increased in patients with SPMS, and resistin is also increased in patients with PPMS. Given that inflammation occurs at a variable intensity from the onset of the disease and that neurodegeneration process starts after disease initiation, in this context the adipokines produced by lipid tissue constitute an additional element in the neuroimmunomodulation complex of organisms with MS (see text for further explanation); thus the adipokines produced constitute an additional element in the neuroimmunomodulation complex of organisms with MS (see text for further explanation). RRMS, Remittent Recurrent Multiple Sclerosis. SPMS, Secondary Progressive Multiple Sclerosis. PPMS, Primary Progressive Multiple Sclerosis. CSF, CerebroSpinal Fluid. Resistin (serum) [–34]. Adipsin (in CSF) [35]. Leptin (serum and CSF) [35]. Adiponectin (in serum) [32, 36, 37]. Chemerin (serum) [38]. A-FABP, Adipocyte-Fatty Acid-Binding Protein (in serum) [39].
Figure 2
Figure 2
Cross talk among immune, neural, and adipose tissues. Adipocytes release leptin, resistin, and visfatin, which induce a low-grade inflammatory state in patients with multiple sclerosis (MS) with obesity. T cells migrate into the Central Nervous System (CNS), with Th1/Th17 cell release of proinflammatory cytokines, which promote the inflammatory status, and Th2/Treg release of anti-inflammatory cytokines, which contributes to modulating the severity of multiple sclerosis (MS). Neurons and oligodendrocytes are those mainly affected in MS. Axons are demyelinated by cell- and molecular-mediated mechanisms. Antigen presentation between microglia and CNS-infiltrating T cells induces a proinflammatory positive feedback loop. Astrocytes costimulate CNS-infiltrating T cells through CD24 expression.
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References

    1. Moroni L., Bianchi I., Lleo A. Geoepidemiology, gender and autoimmune disease. Autoimmunity Reviews. 2012;11(6-7):A386–A392. doi: 10.1016/j.autrev.2011.11.012. - DOI - PubMed
    1. Versini M., Jeandel P.-Y., Rosenthal E., Shoenfeld Y. Obesity in autoimmune diseases: not a passive bystander. Autoimmunity Reviews. 2014;13(9):981–1000. doi: 10.1016/j.autrev.2014.07.001. - DOI - PubMed
    1. WHO. Overweight/obesity: overweight by country. Global Health Observatory Data Repository 2008–2013. 2016, http://www.who.int/gho/ncd/risk_factors/obesity_text/en/
    1. Gremese E., Tolusso B., Gigante M. R., Ferraccioli G. Obesity as a risk and severity factor in rheumatic diseases (autoimmune chronic inflammatory diseases) Frontiers in Immunology. 2014;5, article 576 doi: 10.3389/fimmu.2014.00576. - DOI - PMC - PubMed
    1. Overs S., Hughes C. M., Haselkorn J. K., Turner A. P. Modifiable comorbidities and disability in multiple sclerosis. Current Neurology and Neuroscience Reports. 2012;12(5):610–617. doi: 10.1007/s11910-012-0293-4. - DOI - PubMed

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