High-fructose corn syrup causes vascular dysfunction associated with metabolic disturbance in rats: Protective effect of resveratrol

Akar, Fatma; Uludag, Orhan; Aydın, Ali; Aytekin, Yasin Atacan; Elbeğ, Şehri; Tuzcu, Mehmet; Şahin, Kazım

doi:10.1016/j.fct.2012.03.061

Cited by 67 publications

(63 citation statements)

References 34 publications

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“…In addition, the control females appeared to have more omental fat mass than males, signifying the gender characteristics. In our previous studies, the weight gaining has not been established in male rats consumed 10% HFCS in drinking water for 10-12 weeks [10,11]. The discrepancy between these former and the present studies can be explained by the differences in experimental protocol design, in particular with feeding durations to induce metabolic disorder as well as the mixture of HFCS that contains 56% fructose and 37% glucose.…”

Section: Discussioncontrasting

confidence: 43%

“…Special care was taken to preserve the endothelium during the preparation of the aortic rings. Functional integrity of the endothelium was checked with the application of acetylcholine (10 -6 M) on phenylephrine (10 -6 M)-precontracted aortic rings and preparations demonstrating <70% relaxations in control rats from both genders were discarded [10,11]. The cumulative concentration-response curves of phenylephrine (10 -9 -10 -4 M) were constructed in the aortic rings.…”

Section: Measurement Of Vascular Reactivity In the Thoracic Aortamentioning

confidence: 99%

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Long-Term Dietary Fructose Causes Gender-Different Metabolic and Vascular Dysfunction in Rats: Modulatory Effects of Resveratrol

Pektaş¹,

Sadı²,

Akar

2015

Cell Physiol Biochem

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Background/Aims: There is limited knowledge on the gender differences in the effects of dietary fructose. In the current study, we investigated whether long-term fructose intake impacts metabolic parameters and vascular reactivity differently between male and female rats. Moreover, we tested whether resveratrol has a gender-specific effectiveness on the alterations. Methods: Male and female rats were divided into four groups as control; resveratrol; fructose and resveratrol plus fructose. Fructose was given to the rats as 10% solution in drinking water for 24 weeks. All rats were fed with the standard diet with or without resveratrol. Results: High-fructose diet increased plasma insulin, triglyceride and VLDL levels as well as omental weights in both genders. Long-term dietary fructose causes marked increase in body weight of males, but not females. Dietary fructose impaired endothelial relaxation to acetylcholine and intensified contraction to phenylephrine in the aortas of male and female rats, but differently it also reduced insulin-induced vasodilation in aortas of female rats. These changes were associated with decreased expression levels of endothelial nitric oxide synthase (eNOS) mRNA and protein, but increased in inducible NOS (iNOS), in aortas of male and female rats. Dietary fructose suppressed expression levels of sirtuin 1 (SIRT1) and insulin receptor substrate-2 (IRS-2) mRNA in aortas from female rats. Resveratrol supplementation efficiently restored fructose-induced metabolic and vascular dysfunction in both genders probably by regulating eNOS and iNOS production. Moreover, the augmentations in SIRT1 and IRS-2 mRNA in females and IRS-1 mRNA in males may possibly contribute to the beneficial effects of resveratrol as well. Conclusion: Long-term fructose intake may differently affect metabolic and vascular function between male and female rats, which are modified by resveratrol.

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Section: Discussioncontrasting

confidence: 43%

Section: Measurement Of Vascular Reactivity In the Thoracic Aortamentioning

confidence: 99%

Long-Term Dietary Fructose Causes Gender-Different Metabolic and Vascular Dysfunction in Rats: Modulatory Effects of Resveratrol

Pektaş¹,

Sadı²,

Akar

2015

Cell Physiol Biochem

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“…It is tempting to speculate that the general oxidative stress (TBARS) and local oxidative stress (VAT) [3] present in FRD animals could be one such trigger. This state of FRD-induced high oxidative stress could in turn decrease sirtuin-1 production [25], a NAD + -dependent histone deacetylase that represses PPARc expression [26] and thus inhibits adipogenesis. Therefore, diminished cell sirtuin-1 production would increase PPARc production, thus triggering adipogenesis.…”

Section: Discussionmentioning

confidence: 99%

Excess fructose intake‐induced hypertrophic visceral adipose tissue results from unbalanced precursor cell adipogenic signals

et al. 2013

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We studied the effect of feeding normal adult male rats with a commercial diet supplemented with fructose added to the drinking water (10% w/v; fructose-rich diet, FRD) on the adipogenic capacity of stromal-vascular fraction (SVF) cells isolated from visceral adipose tissue (VAT) pads. Animals received either the commercial diet or FRD ad libitum for 3 weeks; thereafter, we evaluated the in vitro proliferative and adipogenic capacities of their VAT SVF cells. FRD significantly increased plasma insulin, triglyceride and leptin levels, VAT mass/cell size, and the in vitro adipogenic capacity of SVF cells. Flow cytometry studies indicated that the VAT precursor cell population number did not differ between groups; however, the accelerated adipogenic process could result from an imbalance between endogenous pro-and anti-adipogenic SVF cell signals, which are clearly shifted towards the former. The increased insulin milieu and its intracellular mediator (insulin receptor substrate-1) in VAT pads, as well as the enhanced SVF cell expression of Zpf423 and peroxisome proliferator receptor-c2 (all pro-adipogenic modulators), together with a decreased SVF cell concentration of anti-adipogenic factors (pre-adipocyte factor-1 and wingless-type MMTV-10b), strongly supports this assumption. We hypothesize that the VAT mass expansion recorded in FRD rats results from the combination of initial accelerated adipogenesis and final cell hypertrophy. It remains to be determined whether FRD administration over longer periods could perpetuate both processes, or whether cell hypertrophy itself remains responsible for a further VAT mass expansion, as observed in advanced/morbid obesity.

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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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High-fructose corn syrup causes vascular dysfunction associated with metabolic disturbance in rats: Protective effect of resveratrol

Cited by 67 publications

References 34 publications

Long-Term Dietary Fructose Causes Gender-Different Metabolic and Vascular Dysfunction in Rats: Modulatory Effects of Resveratrol

Long-Term Dietary Fructose Causes Gender-Different Metabolic and Vascular Dysfunction in Rats: Modulatory Effects of Resveratrol

Excess fructose intake‐induced hypertrophic visceral adipose tissue results from unbalanced precursor cell adipogenic signals

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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