scholarly journals A cafeteria diet triggers intestinal inflammation and oxidative stress in obese rats

2017 ◽  
Vol 117 (2) ◽  
pp. 218-229 ◽  
Author(s):  
K. Gil-Cardoso ◽  
I. Ginés ◽  
M. Pinent ◽  
A. Ardévol ◽  
X. Terra ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Intestinal Inflammation ◽  
Cafeteria Diet ◽  
Zucker Rats ◽  
Standard Diet ◽  
Metabolic Alterations ◽  
Genetic Obesity ◽  
Obesogenic Diet ◽  
The Impact ◽  
And Oxidative Stress

AbstractThe gastrointestinal alterations associated with the consumption of an obesogenic diet, such as inflammation, permeability impairment and oxidative stress, have been poorly explored in both diet-induced obesity (DIO) and genetic obesity. The aim of the present study was to examine the impact of an obesogenic diet on the gut health status of DIO rats in comparison with the Zucker (fa/fa) rat leptin receptor-deficient model of genetic obesity over time. For this purpose, female Wistar rats (n 48) were administered a standard or a cafeteria diet (CAF diet) for 12, 14·5 or 17 weeks and were compared with fa/fa Zucker rats fed a standard diet for 10 weeks. Morphometric variables, plasma biochemical parameters, myeloperoxidase (MPO) activity and reactive oxygen species (ROS) levels in the ileum were assessed, as well as the expressions of proinflammatory genes (TNF-α and inducible nitric oxide synthase (iNOS)) and intestinal permeability genes (zonula occludens-1, claudin-1 and occludin). Both the nutritional model and the genetic obesity model showed increased body weight and metabolic alterations at the final time point. An increase in intestinal ROS production and MPO activity was observed in the gastrointestinal tracts of rats fed a CAF diet but not in the genetic obesity model. TNF-α was overexpressed in the ileum of both CAF diet and fa/fa groups, and ileal inflammation was associated with the degree of obesity and metabolic alterations. Interestingly, the 17-week CAF group and the fa/fa rats exhibited alterations in the expressions of permeability genes. Relevantly, in the hyperlipidic refined sugar diet model of obesity, the responses to chronic energy overload led to time-dependent increases in gut inflammation and oxidative stress.

scholarly journals The Role of Mitochondria in Sex-Dependent Differences in Hepatic Steatosis and Oxidative Stress in Response to Cafeteria Diet-Induced Obesity in Mice

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1618
Author(s):  
Juliana Morais Mewes ◽  
Fabiana Rodrigues Silva Gasparin ◽  
Tiago Yoshida ◽  
Mariana Amâncio Daniel da Silva ◽  
Maria Raquel Marçal Natali ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Er Stress ◽  
Fatty Acid Oxidation ◽  
Liver Steatosis ◽  
Cafeteria Diet ◽  
Acid Oxidation ◽  
Standard Diet ◽  
Mitochondrial Energy Metabolism ◽  
And Oxidative Stress

Female mice fed a cafeteria diet (FCaf) develop higher liver steatosis and oxidative stress than males (MCaf) as a consequence of unresolved ER stress. Here, we investigated whether mitochondria play a role in this sex difference. The isolated mitochondria from FCaf showed more signs of oxidative stress than those of MCaf, correlated with a reduced content of GSH, increased amount of reactive oxygen species (ROS), and lower activities of enzymes involved in ROS neutralisation. Mitochondria from FCaf and MCaf livers exhibited lower rates of succinate-driven state III respiration and reduced ATPase activity in intact coupled mitochondria compared to their controls fed a standard diet (FC and MC), with no differences between the sexes. Fatty acid oxidation in mitochondria and peroxisomes was higher in MCaf and FCaf compared to their respective controls. In the intact perfused liver, there was no difference between sex or diet regarding the fatty acid oxidation rate. These results indicated that cafeteria diet did not affect mitochondrial energy metabolism, even in FCaf livers, which have higher steatosis and cellular oxidative stress. Nevertheless, the increase in mitochondrial ROS generation associated with a decrease in the antioxidant defence capacity, probably contributes to inducing or reinforcing the ER stress in FCaf livers.

Mercury Exposure and Endothelial Dysfunction

2015 ◽  
Vol 34 (4) ◽  
pp. 300-307 ◽  
Author(s):  
Swati Omanwar ◽  
M. Fahim
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Vascular Endothelium ◽  
Circulatory System ◽  
Vital Role ◽  
Mercury Exposure ◽  
And Function ◽  
The Impact ◽  
And Oxidative Stress

Vascular endothelium plays a vital role in the organization and function of the blood vessel and maintains homeostasis of the circulatory system and normal arterial function. Functional disruption of the endothelium is recognized as the beginning event that triggers the development of consequent cardiovascular disease (CVD) including atherosclerosis and coronary heart disease. There is a growing data associating mercury exposure with endothelial dysfunction and higher risk of CVD. This review explores and evaluates the impact of mercury exposure on CVD and endothelial function, highlighting the interplay of nitric oxide and oxidative stress.

scholarly journals Oxidative Stress Inside the Pathogenesis of Ascending Aorta Aneurysms: A Clearer Vision for Identifying Promising Biomarkers and Therapeutic Targets

2021 ◽  
Author(s):  
Carmela Balistreri ◽  
Calogera Pisano ◽  
Giovanni Ruvolo
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Genetic Variants ◽  
Complex Disease ◽  
Ascending Aorta ◽  
Oxygen Species ◽  
Aorta Aneurysm ◽  
Independent Risk Factors ◽  
The Impact ◽  
And Oxidative Stress

Ascending aorta aneurysm (AsAA) is a complex disease, currently defined an inflammatory disease. In the sporadic form, AsAA has, indeed, a complex physiopathology with a strong inflammatory basis, significantly modulated by genetic variants in innate/inflammatory genes, acting as independent risk factors and as largely evidenced in our recent studies performed during the last 10 years. Based on these premises, here, we want to revise the impact of reactive oxygen species (ROS) and oxidative stress on AsAA pathophysiology and consequently on the onset and progression of sporadic AsAA. This might consent to add other important pieces in the intricate puzzle of the pathophysiology of this disease with the translational aim to identify biomarkers and targets to apply in the complex management of AsAA, by facilitating the AsAA diagnosis currently based only on imaging evaluations, and the treatment exclusively founded on surgery approaches.

scholarly journals The impact of various antihypertensive medications on vascular aging

2021 ◽  
Vol 27 (2) ◽  
pp. 133-145
Author(s):  
E. N. Dudinskaya ◽  
L. V. Matchekhina ◽  
K. A. Eruslanova ◽  
O. A. Dogotar ◽  
L. P. Ryltseva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Pulse Wave ◽  
Antihypertensive Drugs ◽  
Augmentation Index ◽  
Vascular Aging ◽  
Antihypertensive Medications ◽  
The Impact ◽  
Stress Patterns ◽  
And Oxidative Stress

The review summarizes the data of past two decades on the effect of hypertension on vascular aging and considers the effect of chronic inflammation and oxidative stress patterns on the remodeling of cardiovascular system. Clinical studies on the effect of various classes of antihypertensive drugs on age-associated parameters of vascular aging are discussed. These include endothelial dysfunction and arterial assessed by endothelium-dependent vasodilation, pulse wave velocity, augmentation index, cardiovascular index, thickness of the intima-media complex, and so on.

Mycotoxin Deactivator Improves Performance, Antioxidant Status, and Reduces Oxidative Stress in Nursery Pigs Fed Diets Containing Mycotoxins

2021 ◽  
Author(s):  
Erika Vivian Santos ◽  
Dalton Oliveira Fontes ◽  
Mara da Silveira Benfato ◽  
Fernanda Schäfer Hackenharr ◽  
Tiago Salomon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Status ◽  
Control Diet ◽  
Negative Control ◽  
Antioxidant Systems ◽  
Contamination Level ◽  
Standard Diet ◽  
Nursery Pigs ◽  
Inclusion Rate ◽  
The Impact

Abstract Ingestion of mycotoxins can result in many problems, including decreased growth rates and immune suppression. The present study aimed to evaluate the impact of the supplementation of a mycotoxin deactivator composed by adsorbent clay minerals, inactivated fermentation extracts of Saccharomyces cerevisiae, blend of antioxidants, organic acids and botanicals in diets containing added mycotoxins for nursery pigs on their performance and antioxidant status. Ninety pigs weaned with 24 days of age (7.12 ± 0.68 kg of BW) were used. Pigs were housed in pens of 3 animals each according to body weight, litter origin and sex. The dietary treatments consisted of feeding the pigs with: a standard control diet as negative control (NC; mycotoxin levels at accepted regulatory Brazilian Ministry of Agriculture standards Deoxynivalenol (DON): <100 ug/ kg; Zearalenone (ZEA): <20 ug/ kg Fumonisins (FB): <1 mg/ kg); the standard diet added with mycotoxins to reach a low contamination level considered as positive low (PCL-; DON: 900 ug/ kg; ZEA: 100 ug/ kg; FB: 5,000 ug/ kg) without deactivator; a positive low added the deactivator at an inclusion rate of 1 kg/ ton (PCL+); the standard diet added with mycotoxins to reach a high contamination level considered as positive high (PCH-; DON: 4,500 ug/ kg; ZEA: 500 ug/ kg; FB: 18,000 ug/ kg) without the deactivator; and a positive high added the deactivator at an inclusion rate of 5 kg/ ton (PCH+). Pigs were individually weighed at the beginning and at the end of each phase and feed intake recorded based on daily pen intake during the experiment. On d 7, 19, 34 and 43 post-weaning blood samples were drawn for antioxidant analyses. Antioxidant enzymes (glutathione peroxidase (GPx) and total superoxide dismutase (TSOD)), vitamins (Vit A, E, and C), and malondialdehyde (MDA)) were evaluated in erythrocyte and plasma samples. Pigs challenged with mycotoxins presented lower performance traits, decrease in the efficiency of central antioxidant systems (↓GPx, ↓TSOD, ↓Vit A, ↓Vit E and ↓Vit C) and a higher oxidative damage to lipids (↑MDA) when compared to the control and deactivator associated treatments. Our findings showed that the use of a mycotoxin deactivator can mitigate the negative impacts on performance and oxidative stress when animals are subjected to diets contaminated by different levels of mycotoxins.

Evaluation of the effect of cafeteria diet on the kidney Na,K‐ATPase activity, and oxidative stress

2019 ◽  
Vol 120 (11) ◽  
pp. 19052-19063
Author(s):  
Isadora Reis Restier Pinheiro ◽  
Marina Fátima Nunes Melo ◽  
Sarah Vivas Sousa ◽  
Bárbara Gatti Cardoso ◽  
Thaís Marques da Silva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Atpase Activity ◽  
Cafeteria Diet ◽  
And Oxidative Stress

scholarly journals Perfluorooctanesulfonic Acid and Perfluorohexanesulfonic Acid Alter the Blood Lipidome and the Hepatic Proteome in a Murine Model of Diet-Induced Obesity

2020 ◽  
Vol 178 (2) ◽  
pp. 311-324
Author(s):  
Marisa Pfohl ◽  
Lishann Ingram ◽  
Emily Marques ◽  
Adam Auclair ◽  
Benjamin Barlock ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Expression Profiles ◽  
Environmental Toxicants ◽  
High Fat ◽  
High Carbohydrate ◽  
Lipid Species ◽  
Perfluorooctanesulfonic Acid ◽  
The Impact ◽  
And Oxidative Stress

Abstract Perfluoroalkyl substances (PFAS) represent a family of environmental toxicants that have infiltrated the living world. This study explores diet-PFAS interactions and the impact of perfluorooctanesulfonic acid (PFOS) and perfluorohexanesulfonic (PFHxS) on the hepatic proteome and blood lipidomic profiles. Male C57BL/6J mice were fed with either a low-fat diet (10.5% kcal from fat) or a high fat (58% kcal from fat) high carbohydrate (42 g/l) diet with or without PFOS or PFHxS in feed (0.0003% wt/wt) for 29 weeks. Lipidomic, proteomic, and gene expression profiles were determined to explore lipid outcomes and hepatic mechanistic pathways. With administration of a high-fat high-carbohydrate diet, PFOS and PFHxS increased hepatic expression of targets involved in lipid metabolism and oxidative stress. In the blood, PFOS and PFHxS altered serum phosphatidylcholines, phosphatidylethanolamines, plasmogens, sphingomyelins, and triglycerides. Furthermore, oxidized lipid species were enriched in the blood lipidome of PFOS and PFHxS treated mice. These data support the hypothesis that PFOS and PFHxS increase the risk of metabolic and inflammatory disease induced by diet, possibly by inducing dysregulated lipid metabolism and oxidative stress.

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