Fructose and Uric Acid: Is There a Role in Endothelial Function?

Jia, Guanghong; Aroor, Annayya R.; Whaley‐Connell, Adam; Sowers, James R.

doi:10.1007/s11906-014-0434-z

Cited by 53 publications

(56 citation statements)

References 55 publications

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“…These abnormalities are closely associated with the development of CVD (3)(4)(5)9). However, the concentration of fructose used in our experiment and in most animal studies was higher than that consumed by human, thereby increasing significant metabolic changes (1,(28)(29)(30).…”

Section: Discussionmentioning

confidence: 71%

“…Reduction of NO bioavailability, caused by reduced eNOS activity and/or accelerated NO degradation, results in impaired endothelium-dependent vasorelaxation, increased thrombus formation, and progressive atherogenesis (7). There is growing evidence that fructose fed animals exhibited impaired endothelium-dependent relaxation (8)(9)(10)(11) and decreased NO bioavailability (12)(13)(14). High fructose consumption is also reported to induce oxidative and nitrative stress in vascular tissues and that oxidative/nitrative stress seems to play a major role in endothelial dysfunction.…”

Section: Introductionmentioning

confidence: 99%

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Naringin ameliorates endothelial dysfunction in fructose-fed rats

et al. 2018

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Abstract. High fructose consumption is associated with metabolic disorders including hyperglycemia and dyslipidemia, in addition to endothelial dysfunction. Naringin, a flavonoid present in citrus fruit, has been reported to exhibit lipid lowering, antioxidant, and cardiovascular protective properties. Therefore, the present study investigated the effect of naringin on fructose-induced endothelial dysfunction in rats and its underlying mechanisms. Male Sprague-Dawley rats were given 10% fructose in drinking water for 12 weeks, whereas control rats were fed drinking water alone. Naringin (100 mg/kg) was orally administered to fructose fed rats during the last 4 weeks of the study. Following 12 weeks, blood samples were collected for measurement of blood glucose, serum lipid profile and total nitrate/nitrite (NOx). Vascular function was assessed by isometric tension recording. Aortic expression of endothelial nitric oxide synthase (eNOS), phosphorylated eNOS (p-eNOS), and nitrotyrosine were evaluated by western blot analysis. Fructose feeding induced increased levels of blood glucose, total cholesterol, triglyceride, and low density lipoprotein. In rat aortae, fructose reduced acethycholine-induced vasorelaxation, without affecting sodium nitroprusside-induced vasorelaxation. Treatment of fructose-fed rats with naringin restored fructose-induced metabolic alterations and endothelial dysfunction. Fructose-fed rats also exhibited decreased serum NOx level, reduced eNOS and p-eNOS protein expression, and enhanced nitrotyrosine expression in aortae. These alterations were improved by naringin treatment. The results of the present study suggested that naringin treatment preserves endothelium-dependent relaxation in aortae from fructose fed rats. This effect is primarily mediated through an enhanced NO bioavailability via increased eNOS activity and decreased NO inactivated to peroxynitrite in aortae.

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Section: Discussionmentioning

confidence: 71%

Section: Introductionmentioning

confidence: 99%

Naringin ameliorates endothelial dysfunction in fructose-fed rats

et al. 2018

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“…cardiorenal metabolic syndrome; cardiovascular disease; insulin resistance; mammalian target of rapamycin; obesity THE CARDIORENAL METABOLIC syndrome (CRS) consists of a constellation of cardiac, renal, and metabolic disorders, including insulin resistance, obesity, metabolic dyslipidemia, high blood pressure, and evidence of early cardiac and renal disease (28). Epidemiological studies showed that 36.1% of adult men and 32.4% of women in the United States in 2010 had metabolic disorders, often termed the metabolic syndrome (66).…”

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confidence: 99%

Overnutrition, mTOR signaling, and cardiovascular diseases

Jia

Aroor

Martinez‐Lemus

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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101

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The prevalence of obesity and associated medical disorders has increased dramatically in the United States and throughout much of the world in the past decade. Obesity, induced by excess intake of carbohydrates and fats, is a major cause of Type 2 diabetes, hypertension, and the cardiorenal metabolic syndrome. There is emerging evidence that excessive nutrient intake promotes signaling through the mammalian target of rapamycin (mTOR), which, in turn, may lead to alterations of cellular metabolic signaling leading to insulin resistance and obesity-related diseases, such as diabetes, cardiovascular and kidney disease, as well as cancer. While the pivotal role of mTOR signaling in regulating metabolic stress, autophagy, and adaptive immune responses has received increasing attention, there remain many gaps in our knowledge regarding this important nutrient sensor. For example, the precise cellular signaling mechanisms linking excessive nutrient intake and enhanced mTOR signaling with increased cardiovascular and kidney disease, as well as cancer, are not well understood. In this review, we focus on the effects that the interaction between excess intake of nutrients and enhanced mTOR signaling have on the promotion of obesity-associated diseases and potential therapeutic strategies involving targeting mTOR signaling.

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“…IR has been linked to overnutrition and obesity via lipotoxicity, sustained low-grade inflammation, oxidative stress, and endoplasmic reticulum stress [15,16]. Systemic and vascular IR have not only been related to overnutrition, but also specifically to an increased intake of high-fructose corn syrup [17,18]. Furthermore, increased fructose content in the diet has been shown to impair insulin response in the vasculature [17,18].…”

Section: Molecular Effects Of Insulin In the Vasculaturementioning

confidence: 99%

Insulin Resistance and Skeletal Muscle Vasculature: Significance, Assessment and Therapeutic Modulators

Manrique

Sowers

2014

Cardiorenal Med

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Overnutrition and sedentarism are closely related to the alarming incidence of obesity and type 2 diabetes mellitus (DM2) in the Western world. Resistance to the actions of insulin is a common occurrence in conditions such as obesity, hypertension and DM2. In the skeletal muscle vasculature, insulin promotes vasodilation and its own transport across the vascular wall to reach its target tissue. Furthermore, insulin resistance (IR) in the skeletal muscle vasculature results in impaired skeletal muscle glucose uptake and altered whole-body glucose homeostasis. The development of different invasive and noninvasive techniques has allowed the characterization of the actions of insulin and other vasoactive hormones in the skeletal muscle vasculature in both health and disease. Current treatment strategies for DM2 do not necessarily address the impaired effect of insulin in the vasculature. Understanding the effects of insulin and other metabolically active hormones in the vasculature should facilitate the development of new therapeutic strategies targeted at the modulation of IR and improvement of whole-body glucose tolerance. i 2014 S. Karger AG, Basel

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Fructose and Uric Acid: Is There a Role in Endothelial Function?

Cited by 53 publications

References 55 publications

Naringin ameliorates endothelial dysfunction in fructose-fed rats

Naringin ameliorates endothelial dysfunction in fructose-fed rats

Overnutrition, mTOR signaling, and cardiovascular diseases

Insulin Resistance and Skeletal Muscle Vasculature: Significance, Assessment and Therapeutic Modulators

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