Postprandial oxidative stress is modified by dietary fat: evidence from a human intervention study

2010 ◽  
Vol 119 (6) ◽  
pp. 251-261 ◽  
Author(s):  
Pablo Perez-Martinez ◽  
Jose Maria Garcia-Quintana ◽  
Elena M. Yubero-Serrano ◽  
Inmaculada Tasset-Cuevas ◽  
Isaac Tunez ◽  
...  

Previous evidence supports the concept that increased oxidative stress may play an important role in MetS (metabolic syndrome)-related manifestations. Dietary fat quality has been proposed to be critical in oxidative stress and the pathogenesis of the MetS. In the present study, we investigated whether oxidative stress parameters are affected by diets with different fat quantity and quality during the postprandial state in subjects with the MetS. Patients were randomly assigned to one of four isoenergetic diets distinct in fat quantity and quality for 12 weeks: a high-saturated-fatty-acid (HSFA) diet, a high-mono-unsaturated-fatty-acid (HMUFA) diet and two low-fat/high-complex carbohydrate diets [supplemented with 1.24 g/day of long-chain n−3 polyunsaturated fatty acid (LFHCC n−3) or with 1 g/day of sunflower oil high in oleic acid (LFHCC) as placebo]. The HMUFA diet enhanced postprandial GSH (reduced glutathione) levels and the GSH/GSSH (oxidized glutathione) ratio, compared with the other three diets. In addition, after the HMUFA-rich diet postprandial lipid peroxide levels, protein carbonyl concentrations, SOD (superoxide dismutase) activity and plasma H2O2 levels were lower compared with subjects adhering to the HSFA-rich diet. Both LFHCC diets had an intermediate effect relative to the HMUFA and HSFA diets. In conclusion, our data support the notion that the HMUFA diet improves postprandial oxidative stress in patients with the MetS. These findings suggest that the postprandial state is important for understanding the possible cardioprotective effects associated with mono-unsaturated dietary fat, particularly in subjects with the MetS.

2012 ◽  
Vol 44 (22) ◽  
pp. 1073-1089 ◽  
Author(s):  
M. J. J. Ronis ◽  
J. N. Baumgardner ◽  
J. C. Marecki ◽  
L. Hennings ◽  
X. Wu ◽  
...  

To determine if dietary fat composition affects the progression of nonalcoholic fatty liver disease (NAFLD), we overfed male Sprague-Dawley rats low (5%) or high (70%) fat diets with different fat sources: olive oil (OO), corn oil (CO), or echium oil (EO), with total enteral nutrition (TEN) for 21 days. Overfeeding of the 5% CO or 5% EO diets resulted in less steatosis than 5% OO ( P < 0.05). Affymetrix array analysis revealed significant differences in hepatic gene expression signatures associated with greater fatty acid synthesis, ChREBP, and SREBP-1c signaling and increased fatty acid transport ( P < 0.05) in the 5% OO compared with 5% CO group. The OO groups had macrosteatosis, but no evidence of oxidative stress or necrosis. The 70% CO and 70% EO groups had a mixture of micro- and macrosteatosis or only microsteatosis, respectively; increased oxidative stress; and increased necrotic injury relative to their respective 5% groups ( P < 0.05). Oxidative stress and necrosis correlated with increasing peroxidizability of the accumulated triglycerides. Affymetrix array analysis comparing the 70% OO and 70% CO groups revealed increased antioxidant pathways and lower expression of genes linked to inflammation and fibrosis in the 70% OO group. A second study in which 70% OO diet was overfed for 50 days produced no evidence of progression of injury beyond simple steatosis. These data suggest that dietary fat type strongly influences the progression of NAFLD and that a Mediterranean diet high in olive oil may reduce the risk of NAFLD progressing to nonalcoholic steatohepatitis.


2021 ◽  
Author(s):  
Xuan Yu ◽  
Xiaocong Zeng ◽  
Feng Xiao ◽  
Ri Chen ◽  
Pritam Sinharoy ◽  
...  

Aims: E-cigarette aerosol containing aldehydes, including acetaldehyde, are metabolized by the enzyme aldehyde dehydrogenase 2 (ALDH2). However, little is known how aldehyde exposure from e-cigarettes, when coupled with an inactivating ALDH2 genetic variant, ALDH2*2 (present in 8% of the world population), affects cardiovascular oxidative stress. The aim of this study was to determine how e-cigarette aerosol exposure, when coupled with genetics, impacts cardiovascular oxidative stress in wild type ALDH2 and ALDH2*2 knock-in mice. Methods and Results: Using selective ion flow mass spectrometry, we determined that e-cigarette aerosol contains acetaldehyde that are 10-fold higher than formaldehyde or acrolein. Next, using wild type ALDH2 and ALDH2*2 knock-in rodents, we identified organ-specific differences in ALDH2 with the heart having 1.5-fold less ALDH2 enzyme activity relative to the liver and lung. In isolated cardiac myocytes, acetaldehyde exposure (30seconds, 0.1-1μM) caused a 4-fold greater peak in calcium levels for ALDH2*2 relative to ALDH2 cardiomyocytes. ALDH2*2 cardiomyocytes exposed to acetaldehyde also demonstrated a 2-fold increase in ROS production and 2.5-fold increase in 4HNE protein adducts relative to ALDH2 cardiomyocytes. For intact rodents, ALDH2*2 knock-in mice exposed to e-cigarette aerosol had an increased heart rate beginning 5 days after exposure compared to wild type ALDH2 mice (775±30bpm versus 679±33bpm, respectively, *p<0.01, n=7-8 per group). E-cigarette aerosol exposure also exacerbated oxidative stress in ALDH2*2 heart homogenates, including a 1.3-fold higher protein carbonyl level, a 1.7-fold higher lipid peroxide level and 1.5-fold greater phosphorylation of NF-κB relative to wild type ALDH2 homogenates. Conclusions: The increased oxidative stress from e-cigarette aerosol aldehydes triggers the proinflammatory NF-κB pathway. As ALDH2 expression and activity is lower in the heart relative to the lung, the heart could be more susceptible to increases in cardiovascular oxidative stress from e-cigarette aerosol; particularly for those carrying an ALDH2*2 genetic variant which limits acetaldehyde metabolism.


2015 ◽  
Vol 35 (6) ◽  
pp. 635-643 ◽  
Author(s):  
A Kumral ◽  
M Giriş ◽  
M Soluk-Tekkeşin ◽  
V Olgaç ◽  
S Doğru-Abbasoğlu ◽  
...  

Objective: Oxidative stress plays an important role in doxorubicin (DOX)-induced toxicity. Carnosine (CAR) is a dipeptide with antioxidant properties. The aim of this study was to evaluate the decreasing or preventive effect of CAR alone or combination with vitamin E (CAR + Vit E) on DOX-induced toxicity in heart, liver, and brain of rats. Methods: Rats were treated with CAR (250 mg kg−1 day−1; intraperitoneally (i.p.)) or CAR + Vit E (equals 200 mg kg−1 α-tocopherol; once every 3 days; intramuscularly) for 12 consecutive days. On the 8th day of treatment, rats were injected with a single dose of DOX (30 mg kg−1, i.p.). Serum cardiac troponin I (cTnI), urea, and creatinine levels; alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities; and oxidative stress parameters in tissues were measured. We also determined thiobarbituric acid reactive substances, diene conjugate, protein carbonyl (PC), and glutathione levels and antioxidant enzyme activities. Results: DOX resulted in increased serum cTnI, ALT, AST, urea, and creatinine levels and increased lipid peroxide and PC levels in tissues. CAR or CAR + Vit E treatments led to decreases in serum cTnI levels and ALT and AST activities. These treatments reduced prooxidant status and ameloriated histopathologic findings in the examined tissues. Conclusion: Our results may indicate that CAR alone, especially in combination with Vit E, protect against DOX-induced toxicity in heart, liver, and kidney tissues of rats. This was evidenced by improved cardiac, hepatic, and renal markers and restoration of the prooxidant state and amelioration of histopathologic changes.


2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Xiaoqing Chi ◽  
Xiaodan Ma ◽  
Zoushuyi Li ◽  
Yong Zhang ◽  
Yong Wang ◽  
...  

Epigallocatechin-3-gallate (EGCG) is one of the fundamental compounds in green tea. The present study was to evaluate the protective effect of EGCG in oxidative damage and apoptosis induced by hydrogen peroxide (H2O2) in chicken lymphocytes. Results showed that preincubation of lymphocytes with EGCG significantly decreased H2O2-reduced cell viability and apoptotic cells with DNA damage, restored the H2O2-dependent reduction in total antioxidant capacity (T-AOC), glutathione peroxidase (GSH-PX), superoxide dismutase (SOD), glutathione (GSH), and glutathione disulfide (GSSG), and suppressed the increase in intracellular reactive oxygen species (ROS), nitric oxide (NO), nitric oxide synthesis (NOS), malondialdehyde (MDA), lipid peroxide (LPO), and protein carbonyl (Carbonyl). In addition, preincubation of the cells with EGCG increased mitochondrial membrane potential (MMP) and reduced calcium ion ([Ca2+]i) load. The protective effect of EGCG in oxidative damage in lymphocytes was accompanied by mRNA expression of SOD, Heme oxygenase-1 (HO-1), Catalase (CAT), GSH-PX, nuclear factor erythroid 2-related factor 2 (Nrf2), and thioredoxin-1 (Trx-1). As EGCG had been removed before lymphocytes were challenged with H2O2, the activation of genes such as Nrf2 and Trx-1 by preincubation with EGCG could be the main reason for EGCG to protect the cells from oxidative damage by H2O2. Since oxidative stress is an important mechanism of biological damage and is regarded as the reasons of several pathologies, the present findings may be helpful for the use of tea products to prevent oxidative stress and maintain healthy in both humans and animals.


2019 ◽  
Vol 97 (Supplement_2) ◽  
pp. 28-28 ◽  
Author(s):  
Charlotte Lauridsen

Abstract Lipids and fatty acids play major roles in relation to mucosal immune responses, epithelial barrier functions, oxidative stress and inflammatory reactions. The composition of fatty acids and their molecular structures (chain length and number of double bonds) influences digestion, absorption and metabolism of the dietary fat, as well as the bioactivity of the fatty acids. Piglets post weaning having immature intestines and immune functions are very vulnerable towards invading microorganisms. Manipulation of the milk fatty acid composition via the sow nutrition, or inclusion of dietary fat sources in the feed, may be used as a strategic tool to enhance pig performance and their gut health pre- and post weaning. Medium-chained fatty acids (MCFA) are absorbed directly into the portal blood and may contribute with immediate energy for the piglet. In addition, the MCFA possess antibacterial effects. The essential fatty acids, linoleic and linolenic fatty acids, form the building blocks for the longer –chained polyunsaturated n-3 and n-6 fatty acids. Their conversion into n-3 and n-6 eicosanoids influence the inflammatory reactions and the immune responses upon bacterial challenge. The proportion of unsaturated fatty acids in the cell membranes influence the susceptibility to oxidative stress. Oxidative stress accompanies infectious diseases, and if uncontrolled, the development of the lipid peroxides may be harmful for the epithelial barrier function. The aim of this presentation is to review how dietary fatty acid composition during critical phases of pigs’ lives can support a normal immune system and modulate resistance to infectious diseases of pigs, and influence growth of the pig. Furthermore, factors that can enhance oxidative stress (e.g. polyunsaturated fatty acids), uncontrolled inflammatory reactions (e.g. high ratio of n-6 to n-3 fatty acids in cellular membranes), and limit immune development (such as deficiency of fat-soluble vitamins), and be harmful for the pig gut health are addressed.


2019 ◽  
Vol 244 (18) ◽  
pp. 1629-1641 ◽  
Author(s):  
Sunmin Park ◽  
Song Mi Cho ◽  
Bo Ram Jin ◽  
Hye Jeong Yang ◽  
Qiu Jing Yi

We hypothesized that a mixture of blackberry fruit and leaf extracts may alleviate non-alcoholic fatty liver disease (NAFLD). Rats with diet-induced NAFLD were used to test the hypothesis and explore possible mechanisms. Male Sprague–Dawley rats were orally administered diets 51% of energy from fat and 450 mg dextrin/kg bw (NAFLD-control), 50% ethanol blackberry leaf extract (450 mg/kg bw; BL), 50% ethanol blackberry fruit extract (450 mg/kg bw; BF), the mixture of blackberry leaf and fruit extracts (2:1; 150 mg/kg bw; BLF), and milk thistle extracts (150 mg/kg bw; positive-control) for 12 weeks. Normal-control rats were fed low-fat diets with 450 mg dextrin/kg bw (20 En% fat diet) Body weight, visceral fat mass, liver triglycerides, serum cholesterol, triglyceride, non-esterified fatty acid, and insulin resistance were all elevated in rats in the NAFLD-control group compared to the normal-controls. Rats in the NAFLD-control group exhibited liver damage accompanied by increased oxidative stress and inflammation compared to the rats in the normal-control group. BL and BLF protected the NAFLD rats against the triglyceride and lipid peroxide accumulation, improved insulin sensitivity and dyslipidemia, and increased the antioxidant enzymes, SOD, and GSH-Px, to levels similar to the normal-control group. Further, BL and BLF ameliorated inflammation and hepatocyte damage compared to the NAFLD-controls, and they suppressed mRNA expressions of genes involved in triglyceride synthesis (FAS and SREBP-1c). BLF also modulated the gut microbiota by elevating Lactobacillus and Akkermansia in the feces from the cecum compared to the NAFLD-control group. The integrity of intestinal tissues was improved, and the number of goblet cells was elevated by BLF. In conclusion, BL and BLF prevented high-fat diet-induced liver damage by protecting against oxidation and inflammation-induced injury. BLF (human equivalent 1.3 g/day) might, therefore, be used as a therapeutic agent for NAFLD. Impact statement NAFLD is a diet-related metabolic disease with no good drug treatments. Therefore, dietary interventions are needed to alleviate NAFLD. This paper demonstrated that feeding a blackberry leaf and fruit mixture extract can alleviate diet-induced NAFLD in rats. Specifically, the blackberry extract, rich in flavonoids and anthocyanins decreased hepatic triglycerides and lipid peroxides, increased genes related to beta oxidation, decreased those involved fatty acid biosynthesis, alleviated oxidative stress, and suppressed pro-inflammatory cytokine release. The blackberry extract also alleviated gut dysbiosis that was associated with NAFLD by increasing the amount of Lactobacillus and Akkermansia in the feces. This research demonstrated that the extract of a common and inexpensive fruit can help alleviate NAFLD and associated intestinal dysbiosis at a dose equivalent to 1.3 g/day in humans. If this work can be duplicated in humans, it would provide a safe and inexpensive intervention to help alleviate NAFLD.


2008 ◽  
Vol 3 ◽  
pp. 33
Author(s):  
E. Garcia-Fuentes ◽  
J.M. Garcia-Almeida ◽  
M. Murri-Pierri ◽  
F. Vilchez ◽  
J. Garcia-Arnes ◽  
...  

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1893-P
Author(s):  
AMBER B. COURVILLE ◽  
SHANNA BERNSTEIN ◽  
MIRELLA GALVAN-DE LA CRUZ ◽  
ANTHONY ONUZURUIKE ◽  
NIRUPA R. MATTHAN ◽  
...  

1961 ◽  
Vol 20 (4) ◽  
pp. 712-717 ◽  
Author(s):  
R. L. Edwards ◽  
S. B. Tove ◽  
T. N. Blumer ◽  
E. R. Barrick

Author(s):  
EJ King ◽  
A Hugo ◽  
FH De Witt ◽  
HJ Van der Merwe ◽  
MD Fair

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