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http://purl.uniprot.org/citations/32268520http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/32268520http://www.w3.org/2000/01/rdf-schema#comment"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-1β, MIP1α, 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."xsd:string
http://purl.uniprot.org/citations/32268520http://purl.org/dc/terms/identifier"doi:10.3390/nu12041006"xsd:string
http://purl.uniprot.org/citations/32268520http://purl.uniprot.org/core/author"Pino J."xsd:string
http://purl.uniprot.org/citations/32268520http://purl.uniprot.org/core/author"Conde J."xsd:string
http://purl.uniprot.org/citations/32268520http://purl.uniprot.org/core/author"Gonzalez-Gay M.A."xsd:string
http://purl.uniprot.org/citations/32268520http://purl.uniprot.org/core/author"Dieguez C."xsd:string
http://purl.uniprot.org/citations/32268520http://purl.uniprot.org/core/author"Tovar S."xsd:string
http://purl.uniprot.org/citations/32268520http://purl.uniprot.org/core/author"Gualillo O."xsd:string
http://purl.uniprot.org/citations/32268520http://purl.uniprot.org/core/author"Lago F."xsd:string
http://purl.uniprot.org/citations/32268520http://purl.uniprot.org/core/author"Mera A."xsd:string
http://purl.uniprot.org/citations/32268520http://purl.uniprot.org/core/author"Francisco V."xsd:string
http://purl.uniprot.org/citations/32268520http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/32268520http://purl.uniprot.org/core/name"Nutrients"xsd:string
http://purl.uniprot.org/citations/32268520http://purl.uniprot.org/core/pages"E1006"xsd:string
http://purl.uniprot.org/citations/32268520http://purl.uniprot.org/core/title"Levels of the Novel Endogenous Antagonist of Ghrelin Receptor, Liver-Enriched Antimicrobial Peptide-2, in Patients with Rheumatoid Arthritis."xsd:string
http://purl.uniprot.org/citations/32268520http://purl.uniprot.org/core/volume"12"xsd:string
http://purl.uniprot.org/citations/32268520http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/32268520
http://purl.uniprot.org/citations/32268520http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/32268520
http://purl.uniprot.org/uniprot/#_Q969E1-mappedCitation-32268520http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32268520
http://purl.uniprot.org/uniprot/#_Q7Z5F5-mappedCitation-32268520http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32268520
http://purl.uniprot.org/uniprot/Q969E1http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/32268520
http://purl.uniprot.org/uniprot/Q7Z5F5http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/32268520