Author, as appears in the article.: Aragones, Gemma; Saavedra, Paula; Heras, Mercedes; Cabre, Anna; Girona, Josefa; Masana, Lluis
Department: Medicina i Cirurgia Ciències Mèdiques Bàsiques
URV's Author/s: ARAGONÈS BARGALLÓ, GEMMA / Aragonès Bargalló, Gerard / CABRÉ LLOBET, ANNA / Girona Tell, Josefa / HERAS IBAÑEZ, MERCEDES / Masana Marín, Luis / SAAVEDRA GARCIA, PAULA
Keywords: Time factors Signal transduction Rna, messenger Resistance Proto-oncogene proteins c-akt Plasma fatty-acid-binding-protein-4 Phosphorylation Nos3 protein, human Nitric oxide synthase type iii Nitric oxide (no) Nitric oxide Metabolic syndrome Mechanisms Irs1 protein, human Insulin-signalling pathway Insulin receptor substrate proteins Insulin Humans Human umbilical vein endothelial cells Heart Gene expression regulation, enzymologic Fatty acid-binding proteins Fatty acid-binding protein 4 (fabp4) Fabp4 protein, human Expression Enzyme activation Endothelium Endothelial nitric oxide synthase (enos) Endothelial dysfunction Dysfunction Diabetes Coronary-artery-disease Cells, cultured Atherosclerosis Adipose-tissue depots
Abstract: Background: Recent studies have shown that fatty acid-binding protein 4 (FABP4) plasma levels are associated with impaired endothelial function in type 2 diabetes (T2D). In this work, we analysed the effect of FABP4 on the insulin-mediated nitric oxide (NO) production by endothelial cells in vitro.Methods: In human umbilical vascular endothelial cells (HUVECs), we measured the effects of FABP4 on the insulin-mediated endothelial nitric oxide synthase (eNOS) expression and activation and on NO production. We also explored the impact of exogenous FABP4 on the insulin-signalling pathway (insulin receptor substrate 1 (IRS1) and Akt).Results: We found that eNOS expression and activation and NO production are significantly inhibited by exogenous FABP4 in HUVECs. FABP4 induced an alteration of the insulin-mediated eNOS pathway by inhibiting IRS1 and Akt activation. These results suggest that FABP4 induces endothelial dysfunction by inhibiting the activation of the insulin-signalling pathway resulting in decreased eNOS activation and NO production.Conclusion: These findings provide a mechanistic linkage between FABP4 and impaired endothelial function in diabetes, which leads to an increased cardiovascular risk. © 2012 Aragonès et al.; licensee BioMed Central Ltd.
Thematic Areas: Saúde coletiva Medicina ii Medicina i Internal medicine Interdisciplinar Farmacia Endocrinology, diabetes and metabolism Endocrinology & metabolism Educação física Ciências biológicas ii Ciências biológicas i Cardiology and cardiovascular medicine Cardiac & cardiovascular systems Biotecnología
licence for use: https://creativecommons.org/licenses/by/3.0/es/
ISSN: 14752840
Author's mail: josefa.girona@urv.cat josefa.girona@urv.cat gerard.aragones@urv.cat luis.masana@urv.cat
Author identifier: 0000-0002-6267-8779 0000-0002-6267-8779 0000-0001-8657-5726 0000-0002-0789-4954
Record's date: 2025-02-08
Paper version: info:eu-repo/semantics/publishedVersion
Licence document URL: https://repositori.urv.cat/ca/proteccio-de-dades/
Paper original source: Cardiovascular Diabetology. 11 72-
APA: Aragones, Gemma; Saavedra, Paula; Heras, Mercedes; Cabre, Anna; Girona, Josefa; Masana, Lluis (2012). Fatty acid-binding protein 4 impairs the insulin-dependent nitric oxide pathway in vascular endothelial cells. Cardiovascular Diabetology, 11(), 72-. DOI: 10.1186/1475-2840-11-72
Entity: Universitat Rovira i Virgili
Journal publication year: 2012
Publication Type: Journal Publications
Repositori URV