Resistin impairs insulin-evoked vasodilation.
Maria Teresa Gentile1, Carmine Vecchione, Gennaro Marino
1Department of Angio-Cardio-Neurology, Neuromed Institute, Pozzilli, Italy.
Diabetes
|December 11, 2007
Summary
Resistin, a hormone elevated in obesity, impairs insulin-induced vasodilation by disrupting endothelial insulin signaling. This leads to vascular insulin resistance and reduced nitric oxide synthase activity.
Area of Science:
- Endocrinology
- Vascular Biology
- Metabolic Syndrome
Background:
- Vascular dysfunction is a hallmark of obesity.
- Resistin is a hormone significantly elevated in obese individuals.
Purpose of the Study:
- To investigate the vascular effects of resistin, particularly its impact on insulin-mediated vasodilation.
Main Methods:
- Experiments were conducted on mouse aortic and mesenteric segments and cultured endothelial cells.
- Vascular effects were assessed in vitro and in vivo.
- Molecular analyses included immunoprecipitation and Western blotting.
Main Results:
- Resistin impaired insulin-evoked vasodilation dose-dependently by reducing endothelial nitric oxide synthase (eNOS) activity.
- This effect was selective for insulin signaling, not affecting acetylcholine or nitroglycerin-induced vasodilation.
- Resistin disrupted insulin receptor substrate (IRS)-1 phosphorylation, impairing downstream AKT/eNOS signaling.
Conclusions:
- Resistin induces selective vascular insulin resistance.
- It impairs endothelial IRS-1 signaling, leading to reduced eNOS activation and vasodilation.
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