Resveratrol prevents high-fructose corn syrup-induced vascular insulin resistance and dysfunction in rats

Babacanoglu, C.; Yıldırım, Numan; Sadı, Gökhan; Pektaş, Mehmet Bilgehan; Akar, Fatma

doi:10.1016/j.fct.2013.07.026

Cited by 64 publications

(52 citation statements)

References 43 publications

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“…These findings are consistent with previous reports (10,17), which demonstrated that an impaired endothelium function was found in aortic rings of fructose fed animals. The presence of NOS inhibitor L-NNA partially inhibited ACh-induced relaxation in aortic rings of fructose fed rats, indicating that fructose feeding impaired the contribution of NO to endothelium-dependent relaxation in aortic tissues.…”

Section: Discussionsupporting

confidence: 83%

“…Indeed, elevated levels of reactive oxygen species (ROS) cause a decrease in bioavailability of NO and an increase in production of powerful oxidant peroxynitrite that induces eNOS inactivation (15,16). A number of studies reported that decreased eNOS expression and increased nitrotyrosine expression were found in aortae from fructose fed rats (8,17,18). Therefore, the increased oxidative stress and the decreased NO synthesis have been proposed to be involved in high fructose-induced 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: Discussionsupporting

confidence: 83%

Section: Introductionmentioning

confidence: 99%

Naringin ameliorates endothelial dysfunction in fructose-fed rats

et al. 2018

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“…The persistent insulin resistance is a result of an alteration in insulin signaling. Decreased endothelial nitric oxide (NO) synthase (eNOS) can lead to endothelium dysfunction by insulin resistance 26 . Nitric oxide is caused vasodilatation in vessels.…”

Section: Discussionmentioning

confidence: 99%

Lipid Profili, Serum Ürik Asit, Glukoz ve İnsülin Direnci Üzerine Gilbert"s Sendromunun Etkileri

Cüre¹,

Cüre²,

Kırbaş³

et al. 2014

Cukurova Medical Journal

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Purpose: The protective effect of bilirubin on atherosclerotic heart disease in Gilbert's syndrome (GS) is well known.The aim of the study was to evaluate whether the atherosclerotic risk factors such as uric acid (UA), insulin resistance, glucose and lipid profiles are reduced in patients with GS compared with healthy subjects. Material and Methods: Thirty-four male and 38 female a total of 72 GS patients and a similar age group of 72 healthy individuals (34 males and 38 females) were included in the study. Both groups were between 16-45 years old and all patients were were non-smokers and drinkers. The levels of UA, lipids, glucose, insulin and C-reactive protein (CRP) were examined. HOMA-IR index were estimated. Results: GS patient's UA is 4.2 ± 0.8 mg/dL, control group's UA is 4.8 ± 1.1 mg/dL. GS patient's HOMA-IR is 1.8 ± 0.6, control group's HOMA-IR is 2.0 ± 0.4. GS patients had significantly lower levels of UA (p < 0.001), insulin (p = 0.021), HOMA-IR (p = 0.039), triglycerides (TG) (p = 0.005), low-density lipoprotein (LDL) (p = 0.036) and CRP (p = 0.006) compared with the control group. Even insignificantly, GS patients had lower levels of total cholesterol whereas highdensity lipoprotein (HDL) (p < 0.001) was found to be higher. Conclusion: Our results shown that in GS patients, increased bilirubin levels are associated with decrease in UA, insulin, LDL, TG, and increased HDL. In GS patients, low level of UA, insulin and lipid profile may be contributed to cardioprotective effect.

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“…Ketonic monosaccharide and disaccharide sucrose have long been added to Fructose, Glucose and Galactose to improve their biochemical, glycobiological and biological properties [1][2][3][4][5][6][7][8][9][10][11]. Ketonic monosaccharide and disaccharide have begun to replace larger sugars in insulin resistance, obesity, LDL cholesterol, triglycerides, metabolic syndrome, type 2 diabetes and cardiovascular disease because they can impart different properties such as biochemical, glycobiological and biological properties, at the same time, provide property enhancements at lower loadings sugars form a variety of ordered structures on nanometer length scales, allowing them to severe as a ordered matrix for Fructose, Glucose and Galactose which add functionality to the sugars [11][12][13][14][15][16][17][18][19][20][21].…”

Section: Editorialmentioning

confidence: 99%

Molecular Dynamics and Monte Carlo Simulations for Replacement Sugars in Insulin Resistance, Obesity, LDL Cholesterol, Triglycerides, Metabolic Syndrome, Type 2 Diabetes and Cardiovascular Disease: A Glycobiological Study

Heidari¹

2016

J Glycobiol

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EditorialKetonic monosaccharide and disaccharide sucrose have long been added to Fructose, Glucose and Galactose to improve their biochemical, glycobiological and biological properties [1][2][3][4][5][6][7][8][9][10][11]. Ketonic monosaccharide and disaccharide have begun to replace larger sugars in insulin resistance, obesity, LDL cholesterol, triglycerides, metabolic syndrome, type 2 diabetes and cardiovascular disease because they can impart different properties such as biochemical, glycobiological and biological properties, at the same time, provide property enhancements at lower loadings sugars form a variety of ordered structures on nanometer length scales, allowing them to severe as a ordered matrix for Fructose, Glucose and Galactose which add functionality to the sugars [11][12][13][14][15][16][17][18][19][20][21]. Discontinuous molecular dynamics simulation is used to study the phase behavior of Fructose, Glucose and Galactose [22][23][24][25]. Considerable effort has been devoted to theoretical and computational simulation studies of sugars phase behavior [26][27][28][29][30][31]. This editorial describes the models used for phase diagrams of selfassembled mono-tethered nanospheres (TNS) from molecular simulation and comparison to larger sugars. An impressive variety of Fructose, Glucose and Galactose of different sugars and geometries has been synthesized. Also, in this editorial, we aim to predict the assembled structures formed from Fructose, Glucose and Galactose as well as to compare with larger sugars. Moreover, we have developed a model for self-assembled mono-tethered nanospheres (TNS) and perform Brownian Dynamics (BD) simulations to investigate the tendency for these model self-assemble.On the other hand, this editorial is in the use of quantum chemical methods for phase equilibrium. We focus on two computational methods related to thermodynamic and biospectroscopic properties and phase behavior. The first is a conceptually straightforward application in which one uses interaction energies between HighFructose Corn Syrup (HFCS) (Glucose-Fructose, Isoglucose and Glucose-Fructose syrup) molecules obtained from quantum chemistry in Monte-Carlo simulation to compute High-Fructose Corn Syrup (HFCS) (Glucose-Fructose, Isoglucose and Glucose-Fructose syrup) molecules thermodynamic and biospectroscopic properties. This has been done as a two-step process. First, the interactions between HighFructose Corn Syrup (HFCS) (Glucose-Fructose, Isoglucose and Glucose-Fructose syrup) molecules are computed from ab initio quantum chemistry. These energies are fit with a model potential function and then used in simulation. Then, in the second step, ab initio calculations have been used to compute interaction energies 5. Bocarsly ME, Powell ES, Avena NM, Hoebel BG (2010) High-fructose corn syrup causes characteristics of obesity in rats: Increased body weight, body fat and triglyceride levels.

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Resveratrol prevents high-fructose corn syrup-induced vascular insulin resistance and dysfunction in rats

Cited by 64 publications

References 43 publications

Naringin ameliorates endothelial dysfunction in fructose-fed rats

Naringin ameliorates endothelial dysfunction in fructose-fed rats

Lipid Profili, Serum Ürik Asit, Glukoz ve İnsülin Direnci Üzerine Gilbert"s Sendromunun Etkileri

Molecular Dynamics and Monte Carlo Simulations for Replacement Sugars in Insulin Resistance, Obesity, LDL Cholesterol, Triglycerides, Metabolic Syndrome, Type 2 Diabetes and Cardiovascular Disease: A Glycobiological Study

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