Articles producció científica> Medicina i Cirurgia

Fatty acid-binding protein 4 impairs the insulin-dependent nitric oxide pathway in vascular endothelial cells

  • Identification data

    Identifier: imarina:6387020
    Handle: http://hdl.handle.net/20.500.11797/imarina6387020
  • Authors:

    Aragonès G
    Saavedra P
    Heras M
    Cabré A
    Girona J
    Masana L
  • Others:

    Author, as appears in the article.: Aragonès G; Saavedra P; Heras M; Cabré A; Girona J; Masana L
    Department: Medicina i Cirurgia Ciències Mèdiques Bàsiques
    URV's Author/s: ARAGONÈS BARGALLÓ, GEMMA / Girona Tell, Josefa / HERAS IBAÑEZ, MERCEDES / Masana Marín, Luis / SAAVEDRA GARCIA, PAULA
    Keywords: Resistance Plasma fatty-acid-binding-protein-4 Nitric oxide (no) Metabolic syndrome Mechanisms Insulin-signalling pathway Insulin Heart Fatty acid-binding protein 4 (fabp4) Expression Endothelium Endothelial nitric oxide synthase (enos) Endothelial dysfunction Dysfunction Diabetes Coronary-artery-disease 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 luis.masana@urv.cat josefa.girona@urv.cat
    Author identifier: 0000-0002-6267-8779 0000-0002-0789-4954 0000-0002-6267-8779
    Record's date: 2023-05-20
    Papper version: info:eu-repo/semantics/publishedVersion
    Link to the original source: https://cardiab.biomedcentral.com/articles/10.1186/1475-2840-11-72
    Licence document URL: http://repositori.urv.cat/ca/proteccio-de-dades/
    Papper original source: Cardiovascular Diabetology. 11
    APA: Aragonès G; Saavedra P; Heras M; Cabré A; Girona J; Masana L (2012). Fatty acid-binding protein 4 impairs the insulin-dependent nitric oxide pathway in vascular endothelial cells. Cardiovascular Diabetology, 11(), -. DOI: 10.1186/1475-2840-11-72
    Article's DOI: 10.1186/1475-2840-11-72
    Entity: Universitat Rovira i Virgili
    Journal publication year: 2012
    Publication Type: Journal Publications
  • Keywords:

    Cardiac & Cardiovascular Systems,Cardiology and Cardiovascular Medicine,Endocrinology & Metabolism,Endocrinology, Diabetes and Metabolism,Internal Medicine
    Resistance
    Plasma fatty-acid-binding-protein-4
    Nitric oxide (no)
    Metabolic syndrome
    Mechanisms
    Insulin-signalling pathway
    Insulin
    Heart
    Fatty acid-binding protein 4 (fabp4)
    Expression
    Endothelium
    Endothelial nitric oxide synthase (enos)
    Endothelial dysfunction
    Dysfunction
    Diabetes
    Coronary-artery-disease
    Atherosclerosis
    Adipose-tissue depots
    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
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