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Nox2-Derived Superoxide Contributes to Cerebral Vascular Dysfunction in Diet-Induced Obesity
Journal article   Open access   Peer reviewed

Nox2-Derived Superoxide Contributes to Cerebral Vascular Dysfunction in Diet-Induced Obesity

Cynthia M. Lynch, Dale A. Kinzenbaw, Xunxheng Chen, Shanshan Zhan, Erin Mezzetti, Jessica Filosa, Adviye Ergul, Jessica L. Faulkner, Frank M. Faraci and Sean P. Didion
Stroke (1970), Vol.44(11), pp.3195-3201
11/01/2013
DOI: 10.1161/STROKEAHA.113.001366
PMCID: PMC4011083
PMID: 24072007
url
https://doi.org/10.1161/STROKEAHA.113.001366View
Published (Version of record) Open Access

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.
Cardiovascular System & Cardiology Clinical Neurology Life Sciences & Biomedicine Neurosciences & Neurology Peripheral Vascular Disease Science & Technology

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