Abstract
BackgroundTo determine the effects of high sucrose diets on vascular reactivity. We hypothesized that similar to high fat diets (HFD), HSD feeding would lead to increased adiposity resulting in inflammation and oxidative stress-mediated impairment of vasodilation.MethodsMale Sprague-Dawley rats were fed control chow (Chow), HSD or HFD diets for 6 weeks. The role of inflammation and oxidative stress on impaired vasodilation were assessed in isolated mesenteric arterioles.ResultsHSD and HFD induced increased adiposity, oxidative stress and inflammation. HFD rats developed fasting hyperglycemia. Both HSD and HFD rats developed impaired glucose tolerance and hyperleptinemia. Nitric oxide (NO)-mediated vasodilation was significantly attenuated in both HSD and HFD rats but was normalized by treatment with antioxidants or anti-inflammatory drugs. Endothelial NO synthase (eNOS) protein expression was not affected by diet. Sensitivity to NO was reduced since NOS inhibition attenuated vasodilation in Chow rats but did not further impair vasodilation in HSD or HFD rats. Likewise, responsiveness to a NO donor was attenuated in both experimental groups.ConclusionsOxidative stress diminishes vasodilatory responsiveness in HSD and HFD rats through ROS-mediated scavenging of NO and decreased smooth muscle sensitivity to NO. Inflammation also plays a significant role in the impaired vasodilation.
Highlights
To determine the effects of high sucrose diets on vascular reactivity
We hypothesized that feeding rats diets containing high sucrose or high fat for 6 weeks would produce oxidative stress and inflammation leading to endothelial dysfunction and impaired vasodilation in small mesenteric resistance arterioles
The goals of the present study were to 1) demonstrate that rats fed a high sucrose or high fat diet gain more adiposity compared to Chow fed controls, 2) show that Reactive oxygen species (ROS) levels were increased in the plasma as well as in small mesenteric resistance arterioles of high sucrose as well as high fat fed rats, 3) determine if Endothelial Nitric Oxide Synthase (eNOS) protein expression is reduced in rats fed either diet thereby contributing to impaired vasodilation, and 4) test whether ROS or inflammatory pathways are involved in the impaired endothelium-dependent vasodilation that occurs after 6 weeks of high sucrose or high fat intake
Summary
To determine the effects of high sucrose diets on vascular reactivity. We hypothesized that similar to high fat diets (HFD), HSD feeding would lead to increased adiposity resulting in inflammation and oxidative stress-mediated impairment of vasodilation. We hypothesized that feeding rats diets containing high sucrose or high fat for 6 weeks would produce oxidative stress and inflammation leading to endothelial dysfunction and impaired vasodilation in small mesenteric resistance arterioles. The goals of the present study were to 1) demonstrate that rats fed a high sucrose or high fat diet gain more adiposity compared to Chow fed controls, 2) show that ROS levels were increased in the plasma as well as in small mesenteric resistance arterioles of high sucrose as well as high fat fed rats, 3) determine if eNOS protein expression is reduced in rats fed either diet thereby contributing to impaired vasodilation, and 4) test whether ROS or inflammatory pathways are involved in the impaired endothelium-dependent vasodilation that occurs after 6 weeks of high sucrose or high fat intake
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