Postprandial Oxidative Stress Research Articles

Short-Term Effect of Pitavastatin Treatment on Glucose and Lipid Metabolism and Oxidative Stress in Fasting and Postprandial State Using a Test Meal in Japanese Men

Introduction. The objective of this study was to clarify how pitavastatin affects glucose and lipid metabolism, renal function, and oxidative stress. Methods. Ten Japanese men (average age of 33.9 years) were orally administered 2 mg of pitavastatin for 4 weeks. Postprandial glucose, lipoprotein metabolism, and oxidative stress markers were evaluated at 0 and 4 weeks of pitavastatin treatment (2 mg once daily) with a test meal consisting of total calories: 460 kcal, carbohydrates: 56.5 g (226 kcal), protein: 18 g (72 kcal), lipids: 18 g (162 kcal), and NaCl: 1.6 g. Metabolic parameters were measured at 0, 60, and 120 minutes after test meal ingestion. Results. After administration of pitavastatin, serum total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B, arachidonic acid, insulin, and adjusted urinary excretion of uric acid decreased, whereas creatinine clearance (C Cr) and uric acid clearance (C UA) increased. And postprandial versus fasting urine 8-hydroxydeoxyguanosine remained unchanged, while postprandial versus fasting isoprostane decreased after pitavastatin treatment. Next, we compared postprandial glucose and lipid metabolism after test meal ingestion before and after pitavastatin administration. Incremental areas under the curve significantly decreased for triglycerides (P < 0.05) and remnant-like particle cholesterol (P < 0.01), while those for apolipoprotein E (apoE), glucose, insulin, and high-sensitivity C-reactive protein remained unchanged. Conclusion. Pitavastatin improves postprandial oxidative stress along with hyperlipidemia.

Women experience lower postprandial oxidative stress compared to men.

BackgroundWomen have enhanced triglyceride (TAG) removal from the circulation following consumption of high-fat loads, potentially leading to decreased reactive oxygen and nitrogen species (RONS) generation. This may have implications related to long-term health outcomes. We examined the oxidative stress response to high-fat feeding between men and women to determine if women are less prone to postprandial oxidative stress as compared to men.MethodsA total of 49 women (mean age: 31 ± 12 yrs) and 49 men (mean age: 27 ± 9 yrs) consumed a high-fat meal in the morning hours following a 10–12 hour overnight fast. Blood samples were collected before and at 2 and 4 hours after the meal. Samples were analyzed for TAG, various markers of oxidative stress (malondialdehyde [MDA], hydrogen peroxide [H2O2], Advanced Oxidation Protein Products [AOPP], nitrate/nitrite [NOx]), and Trolox-Equivalent Antioxidant Capacity (TEAC). Area under the curve (AUC) was calculated for each variable. Effect size calculations were performed using Cohen’s d. Data from the total sample of 98 subjects were collected as a part of six previously conducted studies in our lab focused on postprandial oxidative stress, between 2007 and 2012.ResultsAUC was higher for men compared to women for TAG (249.0 ± 21.5 vs. 145.0 ± 9.8 mg·dL-1·4 hr-1; p < 0.0001; effect size = 0.89), MDA (2.7 ± 0.2 vs. 2.2 ± 0.1 μmol·L-1·4 hr-1; p = 0.009; effect size = 0.47), H2O2 (29.9 ± 2.4 vs. 22.5 ± 1.6 μmol·L-1·4 hr-1; p = 0.001; effect size = 0.55), AOPP (92.8 ± 6.9 vs. 56.4 ± 3.7 μmol·L-1·4 hr-1; p < 0.0001; effect size = 1.38), and TEAC (1.7 ± 0.1 vs. 1.3 ± 0.0 mmol·L-1·4 hr-1; p = 0.002; effect size = 0.91). No significant difference was noted for NOx (42.2 ± 4.6 vs. 38.3 ± 3.5 μmol·L-1·4 hr-1 for men and women, respectively; p = 0.09; effect size = 0.17).ConclusionIn the context of the current design, women experienced lower postprandial oxidative stress compared to men. Future work is needed to determine the potential health implications of lower postprandial oxidative stress in women.

Postprandial oxidative stress is modulated by dietary fat in adipose tissue from elderly people

We have investigated whether dietary fat modifies the postprandial oxidative stress in adipose tissue of elderly people. Twenty participants received three diets for 4weeks each: SFA-rich diet, Mediterranean (Med) diet enriched in MUFA with virgin olive oil, and a low-fat, high-carbohydrate diet enriched in n-3 PUFA (α-linolenic acid from plant origin) (CHO-PUFA diet). After 12h of fasting, volunteers received a breakfast reflecting the fatty acid composition of the diet ingested in the preceding dietary period. Med diet induced higher postprandial SOD2 and TrxR mRNA levels, and CHO-PUFA diet induced higher GPx1 and TrxR mRNA levels compared with SFA-rich diet. Med and CHO-PUFA breakfasts induced a postprandial increase in plasma reduced glutathione (GSH), and a greater postprandial GSH/oxidized glutathione ratio compared to the SFA-rich diet. Our study suggests that the consumption of Med and CHO-PUFA diets may reduce postprandial oxidative stress compared to an SFA-rich diet, which may be due to higher antioxidant enzymes gene expression in adipose tissue.

A beverage of Asiatic plantain extracts alleviated postprandial oxidative stress in overweight hyperlipidemic subjects challenged with a high-fat meal: a preliminary study

There is emerging interest in the potential of the phenolic compounds of Asiatic plantain (Plantago asiatica L.) to attenuate in vitro and in vivo oxidative stress. We hypothesized that a single administration of Asiatic plantain beverage may exert protective effects against postprandial oxidative stress. This preliminary study was designed to compare the ability of different doses of Asiatic plantain beverage to mitigate the postprandial effects of a high-fat meal on the oxidation of lipids and DNA in overweight hyperlipidemic subjects. In a randomized, double-blind, placebo-controlled parallel design (n = 10/group), 40 subjects were administered a single high-fat meal with either a placebo or 1 of 3 Asiatic plantain extract beverages (low, intermediate, or high dose). Blood samples were obtained at fasting and 60, 120, 240, and 360 minutes (total of 5 samples) after intervention. The data showed a tendency for plasma free fatty acid levels to decrease in response to high-dose Asiatic plantain at all time points. Plasma oxidized low-density lipoprotein levels were significantly reduced with high-dose Asiatic plantain at 120 minutes (P = .0251 vs placebo). A comet assay revealed that DNA damage in lymphocytes was significantly decreased by Asiatic plantain at 360 minutes (P = .0225 vs placebo). There were no treatment differences in triglyceride or malondialdehyde levels. The maximum suppression was achieved with a high dose (20 g Asiatic plantain extract/80 mL). These results suggest that by protecting low-density lipoprotein and DNA, an Asiatic plantain beverage may be useful to enhance antioxidant.

Diet Antioxidant Capacity: Relationships to Oxidative Stress and Health

This review will discuss some of the antioxidant assays and biomarkers/measurements used to assess the effect of dietary components on ameliorating in vivo oxidative stress. Although the development of dietary antioxidants has become a major component of the dietary supplement market, this review will focus on foods (primarily fruits and vegetables) and their impact on biomarkers of oxidative stress and the ultimate appearance of disease states. Data is reviewed demonstrating the importance of consumption of dietary antioxidants along with meals to prevent postprandial oxidative stress. Epidemiology studies have demonstrated the relationships between dietary antioxidant intake in the form of polyphenolic type compounds and health outcomes. However, additional research is needed in order to clearly define the mechanism(s) of action of the polyphenolics and whether their effects are direct or indirect in nature.

Influence of Acute Coffee Consumption on Postprandial Oxidative Stress

Background:Coffee has been reported to be rich in antioxidants, with both acute and chronic consumption leading to enhanced blood antioxidant capacity. High-fat feeding is known to result in excess production of reactive oxygen and nitrogen species, promoting a condition of postprandial oxidative stress.Methods:We tested the hypothesis that coffee intake following a high-fat meal would attenuate the typical increase in blood oxidative stress during the acute postprandial period. On 3 different occasions, 16 men and women consumed a high-fat milk shake followed by either 16 ounces of caffeinated or decaffeinated coffee or bottled water. Blood samples were collected before and at 2 and 4 hours following intake of the milk shake and analyzed for triglycerides (TAG), malondialdehyde (MDA), hydrogen peroxide (H2O2), and Trolox equivalent antioxidant capacity (TEAC).Results:Values for TAG and MDA (P < 0.001), as well as for H2O2 (P < 0.001), increased significantly following milk shake consumption, with values higher at 4 hours compared with 2 hours post consumption for TAG and H2O2 (P < 0.05). TEAC was unaffected by the milk shake consumption. Coffee had no impact on TAG, MDA, H2O2, or TEAC, with no condition or interaction effects noted for any variable (P > 0.05).Conclusions:Acute coffee consumption following a high-fat milk shake has no impact on postprandial oxidative stress.

Postprandial oxidative stress and polyphenols

Postprandial oxidative stress and polyphenols

Inhibition of iron-induced lipid peroxidation by newly identified bacterial carotenoids in model gastric conditions: comparison with common carotenoids

Newly identified spore-forming pigmented marine bacteria, Bacillus indicus HU36 and Bacillus firmus GB1, are sources of carotenoids (mainly 15 yellow and orange pigments and 13 pink pigments, respectively) with original structures. These bacterial carotenoids were evaluated for their ability to inhibit the iron-induced peroxidation of linoleic acid micelles, or sunflower oil-in-water emulsions, in comparison with β-carotene, lycopene and astaxanthin. Lipid peroxidation was carried out in acidic conditions and initiated by dietary heme or non-heme iron (metmyoglobin or Fe(II), respectively) so as to simply simulate the postprandial gastric medium, a possible site for dietary oxidative stress. Lipid hydroperoxide formation and carotenoid consumption were followed by UV-vis spectroscopy and appropriate indicators of the antioxidant activity were estimated in each model. The bacterial carotenoids were found to be better inhibitors of heme-induced lipid peroxidation than the reference carotenoids as a likely consequence of their location closer to the interface in micelles and lipid droplets. However, this trend was not confirmed in lipid peroxidation induced by non-heme iron, possibly because of the redox recycling of Fe(II) by carotenoids. The quantitative kinetic analysis of the peroxidation curves suggests that the carotenoids mainly inhibit the propagation phase of lipid peroxidation by direct scavenging of the lipid peroxyl radicals, in agreement with independent experiments showing that carotenoids are unable to reduce the one-electron oxidized form of metmyoglobin (ferrylmyoglobin), a model of initiating species in heme-induced lipid peroxidation. Overall, carotenoids from Bacillus indicus HU36 and Bacillus firmus GB1 were found to be interesting antioxidants to fight postprandial oxidative stress in the stomach.

The antioxidants in oils heated at frying temperature, whether natural or added, could protect against postprandial oxidative stress in obese people

We have investigated the effects of the intake of oils heated at frying temperature in order to find an oil model for deep-frying that prevents postprandial oxidative stress. Twenty obese people received four breakfasts following a randomised crossover design consisting of different oils (virgin olive oil (VOO), sunflower oil (SFO), and a mixed seed oil (SFO/canola oil) with added dimethylpolysiloxane (SOX) or natural antioxidants from olives (SOP)), which were subjected to 20 heating cycles. The intake of SFO-breakfast reduced plasma GSH levels and the GSH/GSSG ratio, increased protein carbonyl levels, and induced a higher gene expression of the different NADPH-oxidase subunits, Nrf2-Keap1 activation, gene expression of the antioxidant enzymes in peripheral blood mononuclear cells and antioxidant plasma activities than the intake of the breakfasts prepared with VOO, SOP and SOX. Oils with phenolic compounds, whether natural (VOO) or artificially added (SOP), or with artificial antioxidant (SOX), could reduce postprandial oxidative stress compared with sunflower oil.

Postprandial changes in the proteome are modulated by dietary fat in patients with metabolic syndrome

Metabolic syndrome is a multicomponent disorder whose etiology is the result of a complex interaction between genetic, metabolic and environmental factors including dietary habits. Our aim was to identify proteome–diet interactions during the postprandial state after the acute intake of four meals with different qualities of fat in the proteome of peripheral blood mononuclear cells. A randomized controlled trial conducted within the LIPGENE study assigned 39 metabolic syndrome patients to one of four meals: a high-saturated-fatty-acid (HSFA) meal, a high-monounsaturated-fatty-acid (HMUFA) meal and two high-polyunsaturated-fatty-acid (from walnut) (HPUFA) meals supplemented with n-3 PUFA or placebo. We analyzed the postprandial changes in the whole proteome of both nuclear and cytoplasmic fractions of peripheral blood mononuclear cells by two-dimensional proteomics. Twenty-three proteins were differentially expressed. HSFA intake caused the postprandial increase of proteins responding to oxidative stress (HSPA1A, PDIA3 and PSME1) and DNA damage (SMC6), whereas HMUFA intake led to the up-regulation of HSPA1A and PDIA3. HPUFA meal supplementation with n-3 PUFA produced peroxisomal beta-oxidation inhibition by down-regulation of ECH1, a process related to insulin signaling improvement. In conclusion, HSFA meal intake causes deleterious postprandial changes in the proteome in terms of DNA damage and procoagulant state, which reflect a higher postprandial oxidative stress after HSFA meal intake as compared to intake of HMUFA and HPUFA meals. Moreover, the addition of long-chain n-3 PUFA to an HPUFA meal may improve insulin signaling and exerts an anti-inflammatory effect when compared to an HPUFA meal.

Dietary Iron-Initiated Lipid Oxidation and Its Inhibition by Polyphenols in Gastric Conditions

The gastric tract may be the first site where food is exposed to postprandial oxidative stress and antioxidant activity by plant micronutrients. After food intake, dietary iron, dioxygen, and emulsified lipids come into close contact and lipid oxidation may take place. This study investigated lipid oxidation and its inhibition by dietary polyphenols in gastric-like conditions. Lipid oxidation induced by heme and nonheme iron was studied in acidic sunflower oil-in-water emulsions. The emulsifier type (bovine serum albumin, phospholipids), pH, and iron form were found to be factors governing the oxidation rates. Quercetin, rutin, and chlorogenic acid highly inhibited the metmyoglobin-initiated lipid oxidation in both emulsified systems at pH 5.8. Additionally, quercetin inhibited nonheme iron-initiated processes, while it was inefficient with hematin as an initiator. The presence of human gastric juice did not influence lipid oxidation, although it diminished the antioxidant activity of phenolics. Model emulsions may thus be valuable tools to study the gastric stability of polyunsaturated lipids.

Grape seed extract attenuates oxidative stress induced by high fat/carbohydrate meal in metabolic syndrome patients

Metabolic syndrome (MS) is associated with increased oxidative stress. Consumption of a high carbohydrate moderate fat (HCMF) meal results in increased markers of postprandial oxidative stress. We hypothesized that grape seed extract (GSE‐Meganatural© Gold), rich in antioxidants would attenuate HCMF meal‐induced oxidative stress in MS. After an overnight fast, 12 subjects with MS (6 men/6 women) consumed a HCMF meal in a randomized cross‐over design. A GSE (300 mg) or placebo capsule was administrated 1 h before the meal. Postprandial changes in plasma lipophilic (LA), hydrophilic (HA) antioxidant status (Oxygen Radical Absorbance Capacity‐ORAC) and oxidized LDL (OX‐LDL) were measured hourly for 6 h. Postprandial plasma ORAC values (LA and HA) measured as area under the curve over 6 hr were significantly increased when the meal was preceded by GSE compared with placebo (P&lt;0.05). Meal‐induced increases in OX‐LDL were attenuated with GSE (P&lt;0.05). These data suggest that the antioxidant activity of GSE produces favorable effects in attenuating oxidative stress in subjects with the MS. Funding: Polyphenolic Inc. Madera, CA

Impact of short-term dietary modification on postprandial oxidative stress

BackgroundWe have recently reported that short-term (21-day) dietary modification in accordance with a stringent vegan diet (i.e., a Daniel Fast) lowers blood lipids as well as biomarkers of oxidative stress. However, this work only involved measurements obtained in a fasted state. In the present study, we determined the postprandial response to a high-fat milkshake with regards to blood triglycerides (TAG), biomarkers of oxidative stress, and hemodynamic variables before and following a 21-day Daniel Fast.MethodsTwenty-two subjects (10 men and 12 women; aged 35 ± 3 years) completed a 21-day Daniel Fast. To induce oxidative stress, a milkshake (fat = 0.8 g·kg-1; carbohydrate = 1.0 g·kg-1; protein = 0.25 g·kg-1) was consumed by subjects on day one and day 22 in a rested and 12-hour fasted state. Before and at 2 and 4 h after consumption of the milkshake, heart rate (HR) and blood pressure were measured. Blood samples were also collected at these times and analyzed for TAG, malondialdehyde (MDA), hydrogen peroxide (H2O2), advanced oxidation protein products (AOPP), nitrate/nitrite (NOx), and Trolox Equivalent Antioxidant Capacity (TEAC).ResultsA time effect was noted for HR (p = 0.006), with values higher at 2 hr post intake of the milkshake as compared to pre intake (p < 0.05). Diastolic blood pressure was lower post fast as compared to pre fast (p = 0.02), and a trend for lower systolic blood pressure was noted (p = 0.07). Time effects were noted for TAG (p = 0.001), MDA (p < 0.0001), H2O2 (p < 0.0001), AOPP (p < 0.0001), and TEAC (p < 0.0001); all concentrations were higher at 2 h and 4 h post intake compared to pre intake, except for TEAC, which was lower at these times (p < 0.05). A condition effect was noted for NOx (p = 0.02), which was higher post fast as compared to pre fast. No pre/post fast × time interactions were noted (p > 0.05), with the area under the curve from pre to post fast reduced only slightly for TAG (11%), MDA (11%), H2O2 (8%), and AOPP (12%), with a 37% increase noted for NOx.ConclusionPartaking in a 21-day Daniel Fast does not result in a statistically significant reduction in postprandial oxidative stress. It is possible that a longer time course of adherence to the Daniel Fast eating plan may be needed to observe significant findings.

Protective activity of processed tomato products on postprandial oxidation and inflammation: A clinical trial in healthy weight men and women

This study was designed to evaluate the ability of tomato rich in lycopene to modify postprandial oxidative stress, inflammation, and endothelial function in healthy weight individuals. Twelve women and 13 men (mean age = 27 ± 8 years; mean body mass index= 22 ± 2) consumed high-fat meals known to induce postprandial oxidative stress on two separate occasions containing either processed tomato product or non-tomato alternative. Blood samples were collected at 0, 30, 60, 90, 120 min, then hourly until 360 min. Flow-mediated dilation (FMD) was performed at 0 and 210 min. Endpoints included changes in glucose, insulin, lipids, oxidized low-density lipoprotein (OxLDL), inflammatory cytokines, and FMD. Both meals induced increases in plasma glucose, insulin, and lipid concentrations (p < 0.05). A trend for higher triglycerides at >240 min was observed after the tomato meal (p = 0.006). Tomato significantly attenuated high-fat meal-induced LDL oxidation (p < 0.05) and rise in interleukin-6 (p < 0.0001), a proinflammatory cytokine and inflammation marker. The data indicate that consuming tomato products with a meal attenuates postprandial lipemia-induced oxidative stress and associated inflammatory response. The relevance of OxLDL and inflammation to vascular injury suggests a potentially important protective role of tomato in reducing cardiovascular disease risk. ClinicalTrials.gov Registration number - NCT00966550.

Antioxidant activity of (all-E)-lycopene and synthetic apo-lycopenoids in a chemical model of oxidative stress in the gastro-intestinal tract

Lycopene, the main pigment of tomato, is known to have protective effects on health. Its metabolites could also be involved in these effects. Potentially bioactive lycopene metabolites namely apo-10′-lycopenol, apo-10′-lycopenal, apo-14′-lycopenol, apo-14′-lycopenal, and apo-11-lycopenoids with alcohol, carboxylic acid, aldehyde and ethyl ester terminal groups were obtained by organic synthesis as (all-E) stereoisomers using HWE condensation reactions. The ability of (all-E)-lycopene and the synthesized apo-lycopenoids to inhibit lipid peroxidation was tested in a chemical model of postprandial oxidative stress in the gastric compartment. Oxidative stress was generated by metmyoglobin, the main form of dietary iron (from red meat), which is able to catalyse the peroxidation of linoleic acid under mildly acidic conditions. In this model, apo-6′-lycopenal and apo-8′-lycopenal were better inhibitors of lipid peroxidation than (all-E)-lycopene itself. For the apo-lycopenoids, a long unsaturated chain and a terminal carboxylic acid group both favour the antioxidant activity. The short-chain apo-lycopenoic acid, apo-14′-lycopenoic acid, was shown to behave like a hydrophilic antioxidant, i.e. by reducing hypervalent iron forms of metmyoglobin. Thus, besides the polyene chain length, the terminal group of the apo-lycopenoids is expected to deeply influence the lipophilic/hydrophilic balance of the molecule (and consequently its distribution between the aqueous and lipid phases) and its affinity for the heme cavity. It can thus be concluded that the polyene chain length and terminal group are two important parameters modulating the mechanism by which apo-lycopenoids express their antioxidant activity.

Inflammatory and Oxidative Stress Responses to High-Carbohydrate and High-Fat Meals in Healthy Humans

The postprandial state is hypothesised to be proinflammatory and prooxidative, but the relative contributions of fat versus carbohydrate are unclear. Therefore, we examined inflammation and oxidative stress responses in serum and skeletal muscle before and after 1000 kcal meals, which were high in either fat or carbohydrate in 15 healthy individuals. Serum and muscle expression of IL6 was elevated 3 hours after each meal, independently of macronutrient composition (P < 0.01). Serum IL18 was decreased after high-fat meal only (P < 0.01). Plasma total antioxidative status and muscle Cu/Zn-superoxide dismutase were decreased after high-carbohydrate meal only (P < 0.05). We conclude that a high-carbohydrate meal may evoke a greater postprandial oxidative stress response, whereas both fat and carbohydrate increased IL6. We speculate that the observed increases in postprandial IL6, without increases in any other markers of inflammation, may indicate a normal IL6 response to enhance glucose uptake, similar to its role postexercise.

Postprandial antioxidant gene expression is modified by Mediterranean diet supplemented with coenzyme Q10 in elderly men and women

Postprandial oxidative stress is characterized by an increased susceptibility of the organism towards oxidative damage after consumption of a meal rich in lipids and/or carbohydrates. We have investigated whether the quality of dietary fat alters postprandial gene expression and protein levels involved in oxidative stress and whether the supplementation with coenzyme Q(10) (CoQ) improves this situation in an elderly population. Twenty participants were randomized to receive three isocaloric diets each for 4weeks: Mediterranean diet supplemented with CoQ (Med + CoQ diet), Mediterranean diet (Med diet), saturated fatty acid-rich diet (SFA diet). After 12-h fast, volunteers consumed a breakfast with a fat composition similar to that consumed in each of the diets. Nrf2, p22(phox) and p47(phox), superoxide dismutase 1 and 2 (SOD1 and SOD2), glutathione peroxidase 1 (GPx1), thiorredoxin reductase (TrxR) gene expression and Kelch-like ECH associating protein 1 (Keap-1) and citoplasmic and nuclear Nrf2 protein levels were determined. Med and Med + CoQ diets induced lower Nrf2, p22(phox), p47(phox), SOD1, SOD2 and TrxR gene expression and higher cytoplasmic Nrf2 and Keap-1 protein levels compared to the SFA diet. Moreover, Med + CoQ diet produced lower postprandial Nrf2 gene expression and lower nuclear Nrf2 protein levels compared to the other diets and lower GPx1 gene expression than the SFA diet. Our results support the antioxidant effect of a Med diet and that exogenous CoQ supplementation has a protective effects against free radical overgeneration through the lowering of postprandial oxidative stress modifying the postprandial antioxidant protein levels and reducing the postprandial expression of antioxidant genes in peripheral blood mononuclear cells.

Changes in markers of inflammation, antioxidant capacity and oxidative stress in smokers following consumption of milk, and milk supplemented with fruit and vegetable extracts and vitamin C

Two milk-based beverages delivering twice the average daily antioxidant intake were formulated, based on synergistic combinations of fruit and vegetable extracts, and containing vitamin C (1.00 mg/ml) for shelf stability. Smokers (n = 42) consumed prototype milk A, B or non-supplemented milk (no extracts or vitamin C; 200 ml) twice daily for 6 weeks. Fasting and post-prandial (2 h after milk consumption) blood samples were collected at baseline and the end of each treatment. Non-supplemented milk significantly reduced fasting inflammatory cytokines (interleukin (IL) 6, IL-1β, tumour necrosis factor-α) compared to baseline. Both supplemented milk-based beverages significantly increased fasting plasma vitamin C concentrations and antioxidant potential and decreased serum uric acid, compared to non-supplemented milk. The beverages did not induce post-prandial oxidative stress or inflammation. Therefore, regular consumption of the supplemented milks may confer health benefits because of increased antioxidant potential or through mechanisms resulting from increased vitamin C or decreased uric acid concentrations.

Drinking Guidance for Red Wine: To Be Taken with Meals: Red Wine Prevents the Postprandial Increase of Plasma Oxidized Lipids

Moderate wine consumption has been shown to lower cardiovascular risk when part of a healthy life style. Red wine compounds, especially polyphenols, might play a role in preventing the development and progression of atherosclerosis, through different modalities of action, including inhibition of lipid peroxidation, metal chelation, free radical scavenging, inhibition of platelet aggregation, anti-inflammatory and estrogenic activity, improvement of endothelial function, lowering of blood pressure and modulation of lipoprotein metabolism. The attenuation of the postprandial oxidative stress could be another mechanism involved in protection by wine phenols, as the absorption of prooxidant/oxidized species with a meal can induce physiological events, such as the formation of mildly oxidized lipoprotein or endothelial dysfunction and inflammatory responses, all linked to the development of cardiovascular disease. As regards oxidizable/oxidized dietary fats, the typical Western diet contains substantial quantities of oxidized lipids. In view of the health implications of their absorption from food, we studied the effect of wine consumption with a meal on modulation of oxidative stress and postprandial increase of plasma oxidized lipids in humans.

Effect of Vitamin C Supplementation on Postprandial Oxidative Stress and Lipid Profile in Type 2 Diabetic Patients

Diabetes mellitus is one of the most wide spread endocrine disorders and an important developing health problem in the world. Cardiovascular disease is a common complication of type 2 diabetes. Several risk factors for coronary heart disease cosegregate in type 2 diabetes, including hyperglycemia, hyperlipaemia, increases production of free radical and decrease in antioxidant defense system. In this study we evaluated the effect of vitamin C supplementation on fasting and postprandial oxidative stress and lipid profile in type 2 diabetic patients. 30 patients with type 2 diabetes from Nader Kazemi Clinic, Shiraz, Iran were randomly divided into 2 groups; vitamin C treatment group (1000 mg d(-1)) and placebo group from May to September 2010. Fasting and postprandial lipid profile and Malondialdehyde (MDA) level were measured at the beginning of the study and after six weeks of supplementation. Data analysis was carried out using Mann-Whitney U test with p < 0.05 being significant by SPSS software version 16.The result of the study showed a significantly decrease in fasting (p = 0.006) and postprandial MDA (p < 0.001) in vitamin C group compare to placebo group but not in lipid profile. This study suggests that vitamin C supplementation can decrease fasting and postprandial oxidative stress and may prevent diabetes complication.