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Do n-3 polyunsaturated fatty acids increase or decrease lipid peroxidation in humans?
Kelley, NS, Yoshida, Y, Erickson, KL
Metabolic syndrome and related disorders. 2014;(8):403-15
Abstract
UNLABELLED Abstract Background: Despite many known health benefits of n-3 polyunsaturated fatty acids (PUFA), there is a concern that their high degree of unsaturation may actually increase oxidative stress, lipid peroxidation (LPO), and chronic inflammatory diseases. METHODS In this review, we have analyzed results from published human studies regarding the effects of n-3 PUFA supplementation on markers of lipid peroxidation. RESULTS Of the 22 published human studies, nine found no change, eight a decrease, and five an increase in markers of LPO. These inconsistencies may be due to methods, subject characteristics, dose, duration, fatty acid and antioxidant composition of supplements, and basal diets. METHODS used for analysis seem to be the most significant factor. Six of eight studies with a decrease in LPO determined F2-isoprostanes produced in vivo, and two determined plasma antioxidant capacity or hydroperoxides. n-3 PUFA can serve as scavengers for free radicals and also modulate expression of genes that determine the balance between oxidative and antioxidative status. Recent studies that monitored oxidation products of cholesterol and fatty acids support the hypothesis that n-3 PUFA decrease LPO. Most of the studies showing no change or increase in LPO determined markers that involved ex vivo sample preparation or oxidation (malondialdehyde, low-density lipoprotein oxidation, lipid hydroperoxides). CONCLUSION A majority of studies do not indicate that n-3 PUFA increased LPO. Future studies need to investigate the effects of dose, duration, and composition of n-3 PUFA with standardized diets and methods on concentrations and types of LPO products produced.
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Low-energy cranberry juice decreases lipid oxidation and increases plasma antioxidant capacity in women with metabolic syndrome.
Basu, A, Betts, NM, Ortiz, J, Simmons, B, Wu, M, Lyons, TJ
Nutrition research (New York, N.Y.). 2011;(3):190-6
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Abstract
Cranberries, high in polyphenols, have been associated with several cardiovascular health benefits, although limited clinical trials have been reported to validate these findings. We tested the hypothesis that commercially available low-energy cranberry juice (Ocean Spray Cranberries, Inc, Lakeville-Middleboro, Mass) will decrease surrogate risk factors of cardiovascular disease, such as lipid oxidation, inflammation, and dyslipidemia, in subjects with metabolic syndrome. In a randomized, double-blind, placebo-controlled trial, participants identified with metabolic syndrome (n = 15-16/group) were assigned to 1 of 2 groups: cranberry juice (480 mL/day) or placebo (480 mL/day) for 8 weeks. Anthropometrics, blood pressure measurements, dietary analyses, and fasting blood draws were conducted at screen and 8 weeks of the study. Cranberry juice significantly increased plasma antioxidant capacity (1.5 ± 0.6 to 2.2 ± 0.4 μmol/L [means ± SD], P < .05) and decreased oxidized low-density lipoprotein and malondialdehyde (120.4 ± 31.0 to 80.4 ± 34.6 U/L and 3.4 ± 1.1 to 1.7 ± 0.7 μmol/L, respectively [means ± SD], P < .05) at 8 weeks vs placebo. However, cranberry juice consumption caused no significant improvements in blood pressure, glucose and lipid profiles, C-reactive protein, and interleukin-6. No changes in these parameters were noted in the placebo group. In conclusion, low-energy cranberry juice (2 cups/day) significantly reduces lipid oxidation and increases plasma antioxidant capacity in women with metabolic syndrome.
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Green tea supplementation affects body weight, lipids, and lipid peroxidation in obese subjects with metabolic syndrome.
Basu, A, Sanchez, K, Leyva, MJ, Wu, M, Betts, NM, Aston, CE, Lyons, TJ
Journal of the American College of Nutrition. 2010;(1):31-40
Abstract
OBJECTIVE To compare the effects of supplementation of green tea beverage or green tea extracts with controls on body weight, glucose and lipid profile, biomarkers of oxidative stress, and safety parameters in obese subjects with metabolic syndrome. DESIGN Randomized, controlled prospective trial. SETTING General Clinical Research Center (GCRC) at University of Oklahoma Health Sciences Center (OUHSC). SUBJECTS Thirty-five subjects with obesity and metabolic syndrome were recruited in age- and gender-matched trios and were randomly assigned to the control (4 cups water/d), green tea (4 cups/d), or green tea extract (2 capsules and 4 cups water/d) group for 8 weeks. The tea and extract groups had similar dosing of epiogallocatechin-3-gallate (EGCG), the active compound in green tea. METHODS Anthropometrics, blood pressure, fasting glucose and lipids, nuclear magnetic resonance (NMR)-based lipid particle size, safety parameters, biomarkers of oxidative stress (oxidized low-density lipoprotein [LDL], myeloperoxidase [MPO], malondialdehyde and hydroxynonenals [MDA and HNE]), and free catechins were analyzed at screen and at 4 and 8 weeks of the study. RESULTS Pairwise comparisons showed green tea beverage and green tea extracts caused a significant decrease in body weight and body mass index (BMI) versus controls at 8 weeks (-2.5 +/- 0.7 kg, p < 0.01, and -1.9 +/- 0.6, p < 0.05, respectively). Green tea beverage showed a decreasing trend in LDL-cholesterol and LDL/high-density lipoprotein (HDL) versus controls (p < 0.1). Green tea beverage also significantly decreased MDA and HNE (-0.39 +/- 0.06 microM, p < 0.0001) versus controls. Plasma free catechins were detectable in both beverage and extract groups versus controls at screen and at 8 weeks, indicating compliance and bioavailability of green tea catechins. CONCLUSIONS Green tea beverage consumption (4 cups/d) or extract supplementation (2 capsules/d) for 8 weeks significantly decreased body weight and BMI. Green tea beverage further lowered lipid peroxidation versus age- and gender-matched controls, suggesting the role of green tea flavonoids in improving features of metabolic syndrome in obese patients.
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Roles of the lipid peroxidation product 4-hydroxynonenal in obesity, the metabolic syndrome, and associated vascular and neurodegenerative disorders.
Mattson, MP
Experimental gerontology. 2009;(10):625-33
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Abstract
A rising tide of obesity and type 2 diabetes has resulted from the development of technologies that have made inexpensive high calorie foods readily available and exercise unnecessary for many people. Obesity and the metabolic syndrome (insulin resistance, visceral adiposity and dyslipidemia) wreak havoc on cells throughout the body thereby promoting cardiovascular and kidney disease, and degenerative diseases of the brain and body. Obesity and insulin resistance promote disease by increasing oxidative damage to proteins, lipids and DNA as the result of a combination of increased free radical production and an impaired ability of cells to detoxify the radicals and repair damaged molecules. By covalently modifying membrane-associated proteins, the membrane lipid peroxidation product 4-hydroxynonenal (HNE) may play particularly sinister roles in the metabolic syndrome and associated disease processes. HNE can damage pancreatic beta cells and can impair the ability of muscle and liver cells to respond to insulin. HNE may promote atherosclerosis by modifying lipoproteins and can cause cardiac cell damage by impairing metabolic enzymes. An adverse role for HNE in the brain in obesity and the metabolic syndrome is suggested by studies showing that HNE levels are increased in brain cells with aging and Alzheimer's disease. HNE can cause the dysfunction and degeneration of neurons by modifying membrane-associated glucose and glutamate transporters, ion-motive ATPases, enzymes involved in amyloid metabolism, and cytoskeletal proteins. Exercise and dietary energy restriction reduce HNE production and may also increase cellular systems for HNE detoxification including glutathione and oxidoreductases. The recent development of low molecular weight molecules that scavenge HNE suggests that HNE can be targeted in the design of drugs for the treatment of obesity, the metabolic syndrome, and associated disorders.
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Dietary soya intake alters plasma antioxidant status and lipid peroxidation in postmenopausal women with the metabolic syndrome.
Azadbakht, L, Kimiagar, M, Mehrabi, Y, Esmaillzadeh, A, Hu, FB, Willett, WC
The British journal of nutrition. 2007;(4):807-13
Abstract
Postmenopausal women with the metabolic syndrome are at high risk of oxidative stress. Several studies have suggested possible antioxidant properties of soya, but little evidence is available regarding the effect of soya on oxidative stress in postmenopausal women with the metabolic syndrome. The objective of the present study was to determine the effects of soya consumption on plasma total antioxidant capacity (TAC) and malondialdehyde (MDA) level in postmenopausal women with the metabolic syndrome. A randomised cross-over trial was undertaken on forty-two postmenopausal women with the metabolic syndrome. Participants were randomly assigned to consume a control (Dietary Approaches to Stop Hypertension; DASH) diet, a soya protein diet, or a soya nut diet, each for 8 weeks. Red meat in the DASH diet (one serving per d) was replaced by soya protein in the soya protein period and by soya nuts in the soya nut period. Significant differences between the end values of the control diet, soya protein diet and soya nut diet were seen for MDA (0.70, 0.64 and 0.63 mumol/l; global P < 0.01). The results also showed a significant difference between the end values for TAC (1950, 2030 and 2110 mumol/l, respectively; P < 0.01). The difference from control for TAC was +4.5 % (P < 0.01) in the soya nut period and +5.8 % (P < 0.01) in the soya protein regimen. Both soya nuts and soya protein decreased MDA significantly compared with the control diet (difference from control was - 7.9 % (P < 0.01) in the soya nut period and - 9.4 % (P < 0.01) in the soya protein diet). We conclude that soya consumption reduces plasma MDA and increases plasma TAC levels in postmenopausal women with the metabolic syndrome.