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Obesity and the risk of Multiple Sclerosis. The role of Leptin

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dc.contributor.author Marrodán, Mariano
dc.contributor.author Farez, Mauricio Franco
dc.contributor.author Balbuena Aguirre, María Eugenia
dc.contributor.author Correale, Jorge
dc.date.accessioned 2021-04-26T12:04:42Z
dc.date.available 2021-04-26T12:04:42Z
dc.date.issued 2021-02
dc.identifier.citation 80. Marrodan M, Farez MF, Balbuena Aguirre ME, Correale J. Obesity and the risk of Multiple Sclerosis. The role of Leptin. Ann Clin Transl Neurol. Ann Clin Transl Neurol. 2021 Feb;8(2):406-424. doi: 10.1002/acn3.51291. Epub 2020 Dec 28. es_ES
dc.identifier.uri https://repositorio.fleni.org.ar/xmlui/handle/123456789/435
dc.identifier.uri https://doi.org/10.1002/acn3.51291
dc.description.abstract Objective: To investigate the effects of leptin on different T-cell populations, in order to gain more insight into the link between leptin and obesity. Methods: Three hundred and nine RRMS patients and 322 controls participated in a cross-sectional survey, to confirm whether excess weight/obesity in adolescence or early adulthood increased the risk of MS. Serum leptin levels were determined by ELISA. MBP83-102 , and MOG63-87 peptide-specific T cells lines were expanded from peripheral blood mononuclear cells. Leptin receptor expression was measured by RT-PCR and flow cytometry. Bcl-2, p-STAT3, pERK1/2, and p27kip1 expression were assayed using ELISA, and apoptosis induction was determined by Annexin V detection. Cytokines were assessed by ELISPOT and ELISA, and regulatory T cells (Tregs) by flow cytometry. Results: Logistic regression analysis, showed excess weight at age 15, and obesity at 20 years of age increased MS risk (OR = 2.16, P = 0.01 and OR = 3.9, P = 0.01). Leptin levels correlated with BMI in both groups. The addition of Leptin increased autoreactive T-cell proliferation, reduced apoptosis induction, and promoted proinflammatory cytokine secretion. Obese patients produced more proinflammatory cytokines compared to overweight/normal/underweight subjects. Inverse correlation was found between leptin levels and circulating Treg cells (r = -0.97, P < 0.0001). Leptin inhibited Treg proliferation. Effects of leptin on CD4+ CD25- effector T cells were mediated by increased STAT3 and ERK1/2 phosphorylation, and down modulation of the cell cycle inhibitor P27kip1 . In contrast, leptin effects on Tregs resulted from decreased phosphorylation of ERK1/2 and upregulation of p27kip1 . Interpretation: Leptin promotes autoreactive T-cell proliferation and proinflammatory cytokine secretion, but inhibits Treg-cell proliferation. es_ES
dc.language.iso eng es_ES
dc.publisher Wiley Periodicals es_ES
dc.rights info:eu-repo/semantics/openAccess
dc.rights.uri https://creativecommons.org/licenses/by/2.5/ar/
dc.subject Multiple Sclerosis es_ES
dc.subject Obesity es_ES
dc.subject Obesidad es_ES
dc.subject Esclerosis Múltiple es_ES
dc.title Obesity and the risk of Multiple Sclerosis. The role of Leptin es_ES
dc.type info:eu-repo/semantics/article es_ES
dc.type info:eu-repo/semantics/publishedVersion
dc.description.fil Fil: Marrodán, Mariano. Fleni. Departamento de Neurología. Servicio de Neuroinmunología y Enfermedades Desmielinizantes; Argentina.
dc.description.fil Fil: Farez, Mauricio Franco. Fleni. Departamento de Neurología; Argentina.
dc.description.fil Fil: Correale, Jorge. Fleni. Departamento de Neurología. Servicio de Neuroinmunología y Enfermedades Desmielinizantes; Argentina.
dc.description.fil Fil: Balbuena Aguirre, María Eugenia. Hospital de Clínicas José de San Martín. Departamento de Neurología; Argentina.
dc.relation.ispartofVOLUME 8
dc.relation.ispartofNUMBER 2
dc.relation.ispartofPAGINATION 406-424
dc.relation.ispartofCOUNTRY Estados Unidos
dc.relation.ispartofCITY Nueva Jersey
dc.relation.ispartofTITLE Annals of clinical and translational neurology
dc.relation.ispartofISSN 2328-9503
dc.type.snrd info:ar-repo/semantics/artículo es_ES


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