Article

Postprandial antioxidant effect of the Mediterranean diet supplemented with coenzyme Q10 in elderly men and women.

Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofia University Hospital/University of Cordoba and CIBER Fisiopatologia Obesidad y Nutricion, Instituto de Salud Carlos III, Spain.
Age (Impact Factor: 3.45). 12/2011; 33(4):579-90. DOI: 10.1007/s11357-010-9199-8
Source: PubMed

ABSTRACT 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 cellular oxidative stress and whether the supplementation with coenzyme Q(10) (CoQ) lowers postprandial oxidative stress in an elderly population. In this randomized crossover study, 20 participants were assigned to receive three isocaloric diets for periods of 4 week each: (1) Mediterranean diet supplemented with CoQ (Med+CoQ diet), (2) Mediterranean diet (Med diet), and (3) saturated fatty acid-rich diet (SFA diet). After a 12-h fast, the volunteers consumed a breakfast with a fat composition similar to that consumed in each of the diets. CoQ, lipid peroxides (LPO), oxidized low-density lipoprotein (oxLDL), protein carbonyl (PC), total nitrite, nitrotyrosine plasma levels, catalase, superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities and ischemic reactive hyperaemia (IRH) were determined. Med diet produced a lower postprandial GPx activity and a lower decrease in total nitrite level compared to the SFA diet. Med and Med+CoQ diets induced a higher postprandial increase in IRH and a lower postprandial LPO, oxLDL, and nitrotyrosine plasma levels than the SFA diet. Moreover, the Med+CoQ diet produced a lower postprandial decrease in total nitrite and a greater decrease in PC levels compared to the other two diets and lower SOD, CAT, and GPx activities than the SFA diet.In conclusion, Med diet reduces postprandial oxidative stress by reducing processes of cellular oxidation and increases the action of the antioxidant system in elderly persons and the administration of CoQ further improves this redox balance.

Full-text

Available from: Francisco Perez-Jimenez, Jun 02, 2015
1 Follower
 · 
227 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Aims: Obesity is characterized by a low-grade systemic inflammatory state and adipose tissue (AT) dysfunction, which predispose individuals to the development of insulin resistance (IR) and metabolic disease. However, a subset of obese individuals, referred to as metabolically healthy obese (MHO) individuals, are protected from obesity-associated metabolic abnormalities. Herein, we aim at identifying molecular factors and pathways in adipocytes responsible for the progression from the insulin-sensitive to the insulin-resistant, metabolically unhealthy obese (MUHO) phenotype. Results: Proteomic analysis of paired samples of adipocytes from subcutaneous (SC) and omental (OM) human adipose tissue revealed that both types of cells are altered in the MUHO state. Specifically, the glutathione redox cycle and other antioxidant defense systems as well as the protein folding machinery were dysregulated and endoplasmic reticulum stress was increased in adipocytes from IR subjects. Moreover, proteasome activity was also compromised in adipocytes of MUHO individuals, which was associated with enhanced accumulation of oxidized and ubiquitinated proteins in these cells. Proteasome activity was also impaired in adipocytes of diet-induced obese mice and in 3T3-L1 adipocytes exposed to palmitate. In line with this data, proteasome inhibition significantly impaired insulin signaling in 3T3-L1 adipocytes. Innovation: This study provides the first evidence of the occurrence of protein homeostasis deregulation in adipocytes in human obesity, which, together with oxidative damage, interferes with insulin signaling in these cells. Conclusion: Our results suggest that proteasomal dysfunction and impaired proteostasis in adipocytes, resulting from protein oxidation and/or misfolding, constitute major pathogenic mechanisms in the development of IR in obesity.
    Antioxidants and Redox Signaling 02/2015; DOI:10.1089/ars.2014.5939 · 7.67 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective: Olive oil protects against cardiovascular disease but the underlying mechanism is still unclear. We speculated that olive oil could inhibit oxidative stress, which is believed to be implicated in the atherosclerotic process. Methods and results: Post-prandial oxidative stress and endothelial dysfunction were investigated in twenty-five healthy subjects who were randomly allocated in a cross-over design to a Mediterranean diet added with or without extra virgin olive oil (EVOO, 10 g) (first study, n = 25) or Mediterranean diet with EVOO (10 g) or corn oil (10 g) (second study, n = 25). Oxidative stress biomarkers including platelet reactive oxidant species (ROS) and 8-iso-PGF2 alpha-III, activity of NOX2, the catalytic sub-unit of NADPH oxidase, as assessed in platelets and serum, serum vitamin E and endothelial dysfunction, were measured before and 2 h after lunch. In the first study a significant increase of platelet ROS, 8-iso-PGF2 alpha-III, NOX2 activity, sE-selectin, sVCAM1 and a decrease of serum vitamin E were detected in controls but not when EVOO was included in the Mediterranean diet; oxidative stress and endothelial dysfunction increase were also observed in the second study in subjects given corn oil. A significant correlation was found between NOX2 activity and platelet oxidative stress. In vitro study demonstrated that EVOO but not corn oil significantly decreased platelet and PMNs oxidative stress and NOX2 activity. Conclusion: The study provides the first evidence that post-prandial oxidative stress may be triggered by NOX2 up-regulation. EVOO but not corn oil, is able to counteract such phenomenon suggesting that addition of EVOO to a Mediterranean diet protects against post-prandial oxidative stress.
    Atherosclerosis 06/2014; 235(2):649-658. DOI:10.1016/j.atherosclerosis.2014.05.954 · 3.97 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: ScopeDietary fat influences systemic inflammatory status, which determines the progression of age-associated diseases. Since somatostatin (SST), cortistatin (CORT) and ghrelin systems modulate inflammatory response, we aim to comprehensively characterize the presence and regulation of the components of these systems in the peripheral blood mononuclear cells (PMBCs), a subset of white blood cells placed at the crossroad between diet and inflammation, in response to diets with different fat composition, and during the postprandial phase in elderly subjects.Methods and resultsThe applied nutrigenomic, inflammation-related PBMC-based approach revealed that the majority of components of SST/CORT and ghrelin systems are present in the human PBMCs. Particularly, CORT, SST/CORT receptors (sst2, sst3, sst5 and sst5TMD4), ghrelin, its acylating enzyme (GOAT), In1-ghrelin variant and GHSR1b were detected in PBMCs. Their expression was altered in the long-term by diet composition, and in the short-term, during the postprandial phase. Of particular relevance is the postprandial elevation of CORT, sst2 and sst5 expression in PBMCs of subjects under n-3 PUFAs-enriched diet.Conclusions Our results suggest a potential relevant role of CORT/ssts and ghrelin systems in regulating PBMCs response to nutrient intake, which could help to explain the positive effects of n-3 PUFAs-enriched diets in reducing the inflammatory response.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 04/2014; 58(9). DOI:10.1002/mnfr.201400059 · 4.91 Impact Factor