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Irisin improves endothelial function in obese mice through the AMPK-eNOS pathway.

Fang Han¹, Shuxian Zhang², Ningning Hou³

¹Department of Pathology, Affiliated Hospital of Weifang Medical University, Weifang, China;

American Journal of Physiology. Heart and Circulatory Physiology

|September 16, 2015

Summary

Irisin, a novel hormone, improves vascular endothelial function in obese mice by activating the AMPK-eNOS pathway. This hormone enhances nitric oxide production and protects against diet-induced endothelial dysfunction.

Keywords:

endothelial function irisin nitric oxide obesity

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Area of Science:

Endocrinology
Vascular Biology
Metabolic Syndrome

Background:

Irisin is a myocyte-secreted hormone linked to endothelial dysfunction in obesity.
Obesity impairs endothelial function, increasing cardiovascular risk.

Purpose of the Study:

To investigate the direct vascular protective effects of irisin on endothelial function in diet-induced obese mice.
To elucidate the underlying molecular mechanisms of irisin's action on the endothelium.

Main Methods:

High-fat diet-induced obesity model in C57BL/6 mice.
Assessment of aortic endothelial function (endothelium-dependent vasodilatation) and nitric oxide (NO) production.
In vitro and in vivo analysis of the AMP-activated protein kinase (AMPK)-Akt-endothelial NO synthase (eNOS) signaling pathway.

Main Results:

Obese mice exhibited significantly impaired endothelium-dependent vasodilatation compared to controls.
Irisin treatment restored endothelial function and enhanced NO production in obese mice.
Irisin's beneficial effects involved the activation of AMPK, Akt, and eNOS phosphorylation, confirmed by inhibitor studies and siRNA suppression of AMPK.

Conclusions:

Irisin demonstrates a direct protective effect on vascular endothelial function in a mouse model of diet-induced obesity.
The mechanism involves the activation of the AMPK-eNOS signaling pathway, leading to improved NO bioavailability.
Irisin represents a potential therapeutic target for managing endothelial dysfunction associated with obesity.