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01.12.2012 | Original investigation | Ausgabe 1/2012 Open Access

Cardiovascular Diabetology 1/2012

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

Zeitschrift:
Cardiovascular Diabetology > Ausgabe 1/2012
Autoren:
Gemma Aragonès, Paula Saavedra, Mercedes Heras, Anna Cabré, Josefa Girona, Lluís Masana
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1475-2840-11-72) contains supplementary material, which is available to authorized users.

Competing interests

Dr. Masana has provided lectures, consultancies and expert testimony to several pharmaceutical companies involved in lipid metabolism, such as Merk Sharp & Dohme, Roche, Esteve, Recordati and Kowa.

Authors’ contribution

GA conducted the experimental work with contributions from JG, GA, PS, MH, AC, JG and LM contributed to method development, establishment of cell lines, experimental design and data interpretation. GA, JG and LM wrote the paper. All authors read and approved the final paper.

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.
Zusatzmaterial
Authors’ original file for figure 1
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Literatur
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