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Leptin-induced endothelial dysfunction in obesity.

Mykhaylo Korda¹, Ruslan Kubant, Stephen Patton

¹Department of Chemistry and Biochemistry, Ohio University, Athens, Ohio 45701-2979, USA.

American Journal of Physiology. Heart and Circulatory Physiology

|August 12, 2008

Summary

High leptin levels in obesity disrupt endothelial nitric oxide (NO) production by increasing eNOS expression and decreasing L-arginine, leading to vascular dysfunction. Supplementation partially restored NO balance in obese mice.

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Area of Science:

Cardiovascular Research
Endothelial Biology
Metabolic Disorders

Background:

Hyperleptinemia associated with obesity negatively impacts endothelial nitric oxide (NO) bioavailability.
This NO dysregulation is a significant contributor to the development of vascular disorders.
Understanding the molecular mechanisms is crucial for addressing obesity-related cardiovascular complications.

Purpose of the Study:

To investigate the effects of leptin on endothelial nitric oxide synthase (eNOS) activity and related reactive species in endothelial cells.
To elucidate the role of hyperleptinemia in obesity-induced endothelial dysfunction in mice.
To explore potential therapeutic interventions for restoring endothelial function.

Main Methods:

Utilized nanosensors to measure nitric oxide (NO), superoxide (O(2)(-)), and peroxynitrite (ONOO(-)) near human umbilical vein endothelial cells (HUVECs) and obese mouse aortic endothelium.
Assessed endothelial nitric oxide synthase (eNOS) expression and L-arginine concentrations.
Investigated the impact of L-arginine and sepiapterin supplementation in obese mice.

Main Results:

Leptin exposure in HUVECs increased eNOS expression, stimulated NO, and elevated cytotoxic O(2)(-) and ONOO(-), decreasing the NO-to-ONOO(-) ratio.
Obese mice exhibited increased leptin, elevated eNOS, and reduced L-arginine, leading to eNOS uncoupling, decreased NO, and increased O(2)(-) and ONOO(-).
Supplementation with L-arginine and sepiapterin reversed eNOS uncoupling and partially restored the NO-to-ONOO(-) balance in obese mice.

Conclusions:

In obesity, leptin promotes eNOS uncoupling and depletes endothelial NO by decreasing L-arginine availability, increasing cytotoxic peroxynitrite.
Hyperleptinemia induces an endothelial NO/ONOO(-) imbalance mirroring dysfunctional endothelium seen in atherosclerosis and diabetes.
L-arginine and sepiapterin supplementation show promise in ameliorating obesity-induced endothelial dysfunction.