The effects of equal caloric high fat and western diet on metabolic syndrome, oxidative stress and vascular endothelial function in mice

2014 ◽  
Vol 211 (3) ◽  
pp. 515-527 ◽  
Author(s):  
I. Heinonen ◽  
P. Rinne ◽  
S. T. Ruohonen ◽  
S. Ruohonen ◽  
M. Ahotupa ◽  
...  
2019 ◽  
Vol 317 (6) ◽  
pp. H1292-H1300 ◽  
Author(s):  
Young-Rae Kim ◽  
Julia S. Jacobs ◽  
Qiuxia Li ◽  
Ravinder Reddy Gaddam ◽  
Ajit Vikram ◽  
...  

SUMOylation is a posttranslational modification of lysine residues. Modification of proteins by small ubiquitin-like modifiers (SUMO)1, -2, and -3 can achieve varied, and often unique, physiological and pathological effects. We looked for SUMO2-specific effects on vascular endothelial function. SUMO2 expression was upregulated in the aortic endothelium of hypercholesterolemic low-density lipoprotein receptor-deficient mice and was responsible for impairment of endothelium-dependent vasorelaxation in these mice. Moreover, overexpression of SUMO2 in aortas ex vivo, in cultured endothelial cells, and transgenically in the endothelium of mice increased vascular oxidative stress and impaired endothelium-dependent vasorelaxation. Conversely, inhibition of SUMO2 impaired physiological endothelium-dependent vasorelaxation in normocholesterolemic mice. These findings indicate that while endogenous SUMO2 is important in maintenance of normal endothelium-dependent vascular function, its upregulation impairs vascular homeostasis and contributes to hypercholesterolemia-induced endothelial dysfunction. NEW & NOTEWORTHY Sumoylation is known to impair vascular function; however, the role of specific SUMOs in the regulation of vascular function is not known. Using multiple complementary approaches, we show that hyper-SUMO2ylation impairs vascular endothelial function and increases vascular oxidative stress, whereas endogenous SUMO2 is essential for maintenance of normal physiological function of the vascular endothelium.


2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 300-300
Author(s):  
Sisi Cao ◽  
William Quarles ◽  
Emily Shaw ◽  
Geoffrey Sasaki ◽  
Priyankar Dey ◽  
...  

Abstract Objectives Observational studies suggest that the regular ingestion of potatoes adversely affects cardiometabolic health, but controlled studies in humans are needed to establish causality. Our objective was to assess whether daily inclusion of non-fried potato foods as part of a Dietary Guidelines for Americans (DGA)-based dietary pattern would impair cardiometabolic health in adults with metabolic syndrome (MetS). Methods In a 2-arm, randomized controlled, crossover trial separated by a 2-wk washout period, MetS adults were provided a eucaloric DGA-based dietary pattern containing potato (350 g with 17.5 g/d resistant starch; POTATO) or an energy-matched bagel (0 g/d resistant starch; CON) for 14 d. Fasting blood was collected on d 0 and 14. On d 14, after a 75 g oral glucose tolerance test, brachial artery flow-mediated dilation (FMD) was measured and blood was collected at 30 min intervals for 2 h to assess vascular endothelial function and metabolic excursions, respectively. Circulating endotoxin, glucose, insulin, and nitric oxide metabolites (NOx) were assessed by spectrophotometry, and malondialdehyde (MDA) and arginine and its metabolites by HPLC. Data were analyzed using two-way repeated measures ANOVA. Results MetS adults (n = 27; 32.5 ± 1.3 y; 35.0 ± 1.0 kg/m2) completed the study with no adverse effects or significant changes in body weight. The 14-d DGA-based dietary pattern had a small but significant effect to decrease glucose (107 ± 1.9 vs. 102 ± 1.7 mg/dL; P = 0.04) and insulin (19 ± 2.9 vs. 14 ± 1.5 μIU/mL; P = 0.03), but these were unaffected by POTATO. Fasting endotoxin, NOx, and MDA and FMD were also unaffected by POTATO compared to CON, as were postprandial AUC0–2h of FMD, insulin, glucose, arginine, MDA, endotoxin, and NOx. Conclusions Findings of this acute controlled trial, which require long-term validation, support that a DGA-based dietary pattern may help to improve insulin resistance and that potatoes can be effectively incorporated into the diet without compromising vascular endothelial function or cardiometabolic health in persons with MetS. Funding Sources Alliance for Potato Research and Education.


2016 ◽  
pp. S515-S518 ◽  
Author(s):  
B. KAPRINAY ◽  
B. LIPTÁK ◽  
L. SLOVÁK ◽  
K. ŠVÍK ◽  
V. KNEZL ◽  
...  

People with metabolic syndrome have higher risk of cardiovascular diseases then those without. The aim of the work was to investigate whether high fat diet administered to Prague hereditary hypertriglyceridemic (HTG) rats can induce signs of metabolic syndrome (MetS). Our results showed that HTG rats fed high fat diet (HTGch) had disturbed glucose metabolism and also lipid metabolism – increased serum triacylglycerols (TAG), total cholesterol (Ch), low-density lipoprotein-Ch (LDL-Ch), and decreased high-density lipoprotein-Ch (HDL-Ch). Their livers proved markers of developing steatosis. Moreover, HTGch had increased blood pressure, yet the vascular endothelium was not significantly damaged. All these changes were accompanied with oxidative stress and tissue damage identified as increased liver concentrations of thiobarbituric acid reactive substances (TBARS) and activity of the lysosomal enzyme N-acetyl-D-glucosaminidase (NAGA). We assume that the model used may be suitable for the study of MetS with no evidence of obesity. Prolongation of the high fat diet duration might have a major impact on all parameters tested, especially on vascular endothelial function.


2017 ◽  
Vol 312 (4) ◽  
pp. H742-H751 ◽  
Author(s):  
Ian Hunter ◽  
Amanda Soler ◽  
Gregory Joseph ◽  
Brenda Hutcheson ◽  
Chastity Bradford ◽  
...  

Thirty percent of the world population is diagnosed with metabolic syndrome. High-fat/high-sucrose (HF/HS) diet (Western diet) correlates with metabolic syndrome prevalence. We characterized effects of the HF/HS diet on vascular (arterial stiffness, vasoreactivity, and coronary collateral development) and cardiac (echocardiography) function, oxidative stress, and inflammation in a rat model of metabolic syndrome (JCR rats). Furthermore, we determined whether male versus female animals were affected differentially by the Western diet. Cardiovascular function in JCR male rats was impaired versus normal Sprague-Dawley (SD) rats. HF/HS diet compromised cardiovascular (dys)function in JCR but not SD male rats. In contrast, cardiovascular function was minimally impaired in JCR female rats on normal chow. However, cardiovascular function in JCR female rats on the HF/HS diet deteriorated to levels comparable to JCR male rats on the HF/HS diet. Similarly, oxidative stress was markedly increased in male but not female JCR rats on normal chow but was equally exacerbated by the HF/HS diet in male and female JCR rats. These results indicate that the Western diet enhances oxidative stress and cardiovascular dysfunction in metabolic syndrome and eliminates the protective effect of female sex on cardiovascular function, implying that both males and females with metabolic syndrome are at equal risk for cardiovascular disease. NEW & NOTEWORTHY Western diet abolished protective effect of sex against cardiovascular disease (CVD) development in premenopausal animals with metabolic syndrome. Western diet accelerates progression of CVD in male and female animals with preexisting metabolic syndrome but not normal animals. Exacerbation of baseline oxidative stress correlates with accelerated progression of CVD in metabolic syndrome animals on Western diet.


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