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Nox2-derived superoxide contributes to cerebral vascular dysfunction in diet-induced obesity. | LitMetric

Nox2-derived superoxide contributes to cerebral vascular dysfunction in diet-induced obesity.

Stroke

From the Departments of Internal Medicine (C.M.L., D.A.K., F.M.F.) and Pharmacology (F.M.F.), The University of Iowa Carver College of Medicine, Iowa City, IA; Vascular Biology Center (X.C., E.M.) and Department of Physiology, Medical College of Georgia (J.F., A.E.), Georgia Regents University, Augusta, GA; Departments of Pharmacology (S.Z., J.L.F., S.P.D.) and Neurology (S.P.D.), The University of Mississippi Medical Center, Jackson, MS; and Charlie Norwood VA Medical Center, Augusta, GA (A.E.).

Published: November 2013

AI Article Synopsis

  • Obesity is a growing global issue, and this study investigates how a high-fat diet (HFD) affects blood flow in the brain and neck arteries, aiming to uncover the underlying mechanisms.
  • In experiments with wild-type and Nox2-deficient mice on HFDs, researchers found that obesity and reduced blood vessel function developed over time, with symptoms appearing sooner in brain arterioles than in carotid arteries.
  • The study highlights that the enzyme Nox2 produces superoxide, which significantly contributes to the endothelial dysfunction observed in wild-type mice, suggesting that these vascular changes may lead to issues with blood flow in obese individuals.

Article Abstract

Background And Purpose: Obesity is an increasing epidemic worldwide; however, little is known about effects of obesity produced by high-fat diet (HFD) on the cerebral circulation. The purpose of this study was to examine the functional and temporal effects of a HFD on carotid and cerebral vascular function and to identify mechanisms that contribute to such functional alterations.

Methods: Responses of cerebral arterioles (in vivo) and carotid arteries (in vitro) were examined in C57Bl/6 (wild-type) and Nox2-deficient (Nox2(-/-)) mice fed a control (10%) or a HFD (45% or 60% kcal of fat) for 8, 12, 30, or 36 weeks.

Results: In wild-type mice, a HFD produced obesity and endothelial dysfunction by 12 and 36 weeks in cerebral arterioles and carotid arteries, respectively. Endothelial function could be significantly improved with Tempol (a superoxide scavenger) treatment in wild-type mice fed a HFD. Despite producing a similar degree of obesity in both wild-type and Nox2(-/-) mice, endothelial dysfunction was observed only in wild-type, but not in Nox2(-/-), mice fed a HFD.

Conclusions: Endothelial dysfunction produced by a HFD occurs in a temporal manner and appears much earlier in cerebral arterioles than in carotid arteries. Genetic studies revealed that Nox2-derived superoxide plays a major role in endothelial dysfunction produced by a HFD. Such functional changes may serve to predispose blood vessels to reduced vasodilator responses and thus may contribute to alterations in cerebral blood flow associated with obesity.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4011083PMC
http://dx.doi.org/10.1161/STROKEAHA.113.001366DOI Listing

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