Levels of the Novel Endogenous Antagonist of Ghrelin Receptor, Liver-Enriched Antimicrobial Peptide-2, in Patients with Rheumatoid Arthritis
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Identificadores![](/xmlui/themes/Mirage2//images/despl_identif.png)
Identificadores
URI: http://hdl.handle.net/20.500.11940/16502
PMID: 32268520
DOI: 10.3390/nu12041006
ISSN: 2072-6643
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Fecha de publicación
2020Título de revista
Nutrients
Tipo de contenido
Journal Article
DeCS
proteínas sanguíneas | citocinas | humanos | péptidos catiónicos antimicrobianos | proteína C reactiva | artritisMeSH
Humans | Cytokines | Antimicrobial Cationic Peptides | C-Reactive Protein | Blood Proteins | ArthritisResumen
Rheumatoid arthritis (RA) is a debilitating, chronic, inflammatory, autoimmune disease associated with cachexia. The substitutive therapy of gut hormone ghrelin has been pointed at as a potential countermeasure for the management of metabolic and inflammatory complications in RA. The recent discovery of liver-expressed antimicrobial peptide 2 (LEAP2) as an endogenous inverse agonist/antagonist of the ghrelin receptor makes feasible the development of a more rational pharmacological approach. This work aimed to assess the serum LEAP2 levels, in a cohort of RA patients, in comparison with healthy individuals and determine its correlation with inflammatory parameters. LEAP2 levels were determined by a commercial ELISA kit, plasma C-reactive protein (CRP) levels were evaluated using immunoturbidimetry, and serum levels of inflammatory mediators, namely IL-6, IL-8, IL-1beta, MIP1alpha, MCP1, and LCN2, were measured by XMap multiplex assay. LEAP2 serum levels were significantly increased in RA patients (n = 101) compared with control subjects (n = 26). Furthermore, the LEAP2 levels significantly correlated with CRP and inflammatory cytokines, but not with BMI. These data reveal LEAP2 as a new potential RA biomarker and indicated the pharmacological control of LEAP2 levels as a novel approach for the treatment of diseases with alterations on the ghrelin levels, such as rheumatoid cachexia.
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