Victor Victor

Universitat de València, Department of Physiology, Faculty Member

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Papers by Victor Victor

The Mitochondria-Targeted Antioxidant MitoQ Modulates Mitochondrial Function and Endoplasmic Reticulum Stress in Pancreatic β Cells Exposed to Hyperglycaemia

Cellular Physiology and Biochemistry, Feb 28, 2019

This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 I... more

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Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Diabetes

Current Pharmaceutical Design, May 5, 2016

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Oxidative Stress, Endothelial Dysfunction and Atherosclerosis

Current Pharmaceutical Design, Sep 1, 2009

This review focuses on the role of oxidative processes in atherosclerosis and the cardiovascular ... more This review focuses on the role of oxidative processes in atherosclerosis and the cardiovascular diseases (CVD) that can arise as a result. Atherosclerosis represents a state of heightened oxidative stress characterized by lipid and protein oxidation in the vascular wall. Overproduction of reactive oxygen species (ROS) under pathophysiologic conditions forms an integral part of the development of CVD, and in particular atherosclerosis. Endothelial dysfunction, characterized by a loss of nitric oxide (NO) bioactivity, occurs early on in the development of atherosclerosis, and determines future vascular complications. Although the molecular mechanisms responsible for mitochondria-mediated disease processes are not clear, oxidative stress seems to play an important role. In general, ROS are essential to the functions of cells, but adequate levels of antioxidant defenses are required in order to avoid the harmful effects of excessive ROS production. In this review, we will provide a summary of the cellular metabolism of reactive oxygen species (ROS) and its role in pathophysiological processes such as atherosclerosis; and currently available antioxidants and possible reasons for their efficacy and inefficacy in ameliorating oxidative stress-mediated diseases.

Mitochondrial impairment and oxidative stress in leukocytes from type 2 diabetic patients

15th International & 14th European Congress of Endocrinology, May 1, 2012

Introduction. Testosterone undecanoate (T) treatment is common in female-to-male transsexuals (Ft... more Introduction. Testosterone undecanoate (T) treatment is common in female-to-male transsexuals (FtMs) but can induce impairment of mitochondrial function and oxidative stress. Aim. The effect of T treatment on the mitochondrial function and redox state of leukocytes of FtMs subjects was evaluated. Methods. This was an observational study conducted in a university hospital. Fifty-seven FtMs were treated with T (1,000 mg) for 12 weeks, after which anthropometric and metabolic parameters and mitochondrial function were evaluated. Main Outcome Measures. Anthropometric and metabolic parameters were evaluated. Mitochondrial function was studied by assessing mitochondrial oxygen (O2) consumption, membrane potential, reactive oxygen species (ROS) production, glutathione levels (GSH), and the reduced glutathione/oxidized glutathione (GSH)/(GSSG) ratio in polymorphonuclear cells. Results. T treatment led to mitochondrial impairment in FtMs as a result of a decrease in mitochondria O2 consumption, the membrane potential, GSH levels, and the (GSH)/(GSSG) ratio and an increase in ROS production. Mitochondrial O2 consumption and membrane potential negatively correlated with T levels, which was further confirmed that the T treatment had induced mitochondrial dysfunction. T also produced a significant increase in total testosterone, free androgenic index, and atherogenic index of plasma, and a decrease in sex hormone-binding globulin and high-density lipoprotein cholesterol. Conclusions. Treatment of FtMs with T can induce impairment of mitochondrial function and a state of oxidative stress. This effect should be taken into account in order to modulate possible comorbidities in these patients. Victor VM, Rocha M, Bañuls C, Rovira-Llopis S, Gómez M, and Hernández-Mijares A. Mitochondrial impairment and oxidative stress in leukocytes after testosterone administration to female-to-male transsexuals.

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Mitochondrial Complex I Impairment in Leukocytes from Polycystic Ovary Syndrome Patients with Insulin Resistance

The Journal of Clinical Endocrinology and Metabolism, Sep 1, 2009

Context: Insulin resistance is a feature of polycystic ovary syndrome (PCOS) and is related to mi... more Context: Insulin resistance is a feature of polycystic ovary syndrome (PCOS) and is related to mitochondrial function. Objective: Our objective was to assess mitochondrial function by evaluating mitochondrial oxygen (O 2) consumption, reactive oxygen species (ROS) production, levels of glutathione (GSH), the oxidized glutathione/GSH ratio, TNF␣ levels, and membrane potential. Additionally, we have evaluated mitochondrial complex I as a target of the oxidative stress responsible for PCOS in polymorphonuclear cells. Design and Setting: This was a prospective controlled study conducted in an academic medical center. Patients: The study population consisted of 20 lean reproductive-age women with PCOS and 20 body composition-matched controls. Main Outcome Measures: We evaluated mitochondrial O 2 consumption using the Clark-type O 2 electrode; levels of ROS, GSH, and membrane potential by means of fluorescence microscopy; TNF␣ levels by ELISA; and complex I activity by spectrophotometric assay. Results: An impairment in mitochondrial function was observed in PCOS patients, evident by a decrease in mitochondrial O 2 consumption; an increase in ROS production, oxidized glutathione/ GSH ratio, and TNF␣ levels; a drop in GSH levels; and an undermining of membrane potential. Furthermore, an impairment of mitochondrial complex I was identified. Conclusion: This study supports the hypothesis of an association between insulin resistance and an impaired mitochondrial oxidative metabolism. We also propose that the oxidative stress responsible for PCOS takes place at complex I. These abnormalities may contribute to the increased risk of type 2 diabetes among women with PCOS.

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The mitochondrial antioxidant SS-31 increases SIRT1 levels and ameliorates inflammation, oxidative stress and leukocyte-endothelium interactions in type 2 diabetes

Scientific reports, Jan 26, 2018

There is growing focus on mitochondrial impairment and cardiovascular diseases (CVD) in type 2 di... more There is growing focus on mitochondrial impairment and cardiovascular diseases (CVD) in type 2 diabetes (T2D), and the development of novel therapeutic strategies in this context. It is unknown whether mitochondrial-targeting antioxidants such as SS-31 protect sufficiently against oxidative damage in diabetes. We aimed to evaluate if SS-31 modulates SIRT1 levels and ameliorates leukocyte-endothelium interactions, oxidative stress and inflammation in T2D patients. Anthropometric and metabolic parameters were studied in 51 T2D patients and 57 controls. Production of mitochondrial reactive oxygen species (ROS), mitochondrial membrane potential, glutathione content, leukocyte-endothelium interactions, NFκB-p65, TNFα and SIRT1 levels was measured in leukocytes treated or not with SS-31. We observed increased mitochondrial ROS production that was restored by SS-31 treatment. SS-31 also increased mitochondrial membrane potential, glutathione content, SIRT1 levels and leukocyte rolling velo...

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The SGLT2 Inhibitor Empagliflozin Ameliorates the Inflammatory Profile in Type 2 Diabetic Patients and Promotes an Antioxidant Response in Leukocytes

Journal of Clinical Medicine, Nov 1, 2019

Sodium-glucose co-transporter 2 inhibitors (iSGLT2) have been linked to a considerable reduction ... more Sodium-glucose co-transporter 2 inhibitors (iSGLT2) have been linked to a considerable reduction in cardiovascular risk in patients with type 2 diabetes (T2D), but the precise molecular mechanisms are still elusive. We aimed to evaluate the effects of the iSGLT2 empagliflozin on systemic inflammation and its potential antioxidant properties. This is an observational, prospective follow-up study of a cohort of fifteen patients with T2D who received 10 mg/day of empagliflozin according to standard clinical care. Measures at baseline, 12 and 24 weeks were taken. Metabolic and anthropometric parameters were evaluated. Production of mitochondrial superoxide, glutathione content, and glutathione s-reductase and catalase mRNA levels were measured in leukocytes. Serum levels of myeloperoxidase, hs-CRP and IL-10 were determined. In addition to decreased body weight and reduced glucose and HbA1c levels, we observed a reduction in superoxide production in leukocytes of diabetic patients and increased glutathione content, prominently after 24 weeks of empagliflozin treatment. Leukocyte expression of glutathione s-reductase and catalase, and serum levels of IL-10 were enhanced at 24 weeks of empagliflozin treatment. Concomitantly, reduced hs-CRP and myeloperoxidase levels were seen. This study provides evidence of the antioxidant and anti-inflammatory properties of empagliflozin treatment in humans, which may contribute to its beneficial cardiovascular effects.

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The Role of Mitochondrial Dynamic Dysfunction in Age-Associated Type 2 Diabetes

The World Journal of Men's Health

Mitochondrial dynamics, such as fusion and fission, play a critical role in maintaining cellular ... more Mitochondrial dynamics, such as fusion and fission, play a critical role in maintaining cellular metabolic homeostasis. The molecular mechanisms underlying these processes include fusion proteins (Mitofusin 1 [MFN1], Mitofusin 2 [MFN2], and optic atrophy 1 [OPA1]) and fission mediators (mitochondrial fission 1 [FIS1] and dynamin-related protein 1 [DRP1]), which interact with each other to ensure mitochondrial quality control. Interestingly, defects in these proteins can lead to the loss of mitochondrial DNA (mtDNA) integrity, impairment of mitochondrial function, a severe alteration of mitochondrial morphology, and eventually cell death. Emerging evidence has revealed a causal relationship between dysregulation of mitochondria dynamics and age-associated type 2 diabetes, a metabolic disease whose rates have reached an alarming epidemic-like level with the majority of cases (59%) recorded in men aged 65 and over. In this sense, fragmentation of mitochondrial networks is often associated with defects in cellular energy production and increased apoptosis, leading, in turn, to excessive reactive oxygen species release, mitochondrial dysfunction, and metabolic alterations, which can ultimately contribute to β-cell dysfunction and insulin resistance. The present review discusses the processes of mitochondrial fusion and fission and their dysfunction in type 2 diabetes, with special attention given to the therapeutic potential of targeting mitochondrial dynamics in this complex metabolic disorder.

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Impact of Roux-en-Y Gastric Bypass on Mitochondrial Biogenesis and Dynamics in Leukocytes of Obese Women

Antioxidants

The chronic low-grade inflammation widely associated with obesity can lead to a prooxidant status... more The chronic low-grade inflammation widely associated with obesity can lead to a prooxidant status that triggers mitochondrial dysfunction. To date, Roux-en-Y gastric bypass (RYGB) is considered the most effective strategy for obese patients. However, little is known about its molecular mechanisms. This interventional study aimed to investigate whether RYGB modulates oxidative stress, inflammation and mitochondrial dynamics in the leukocytes of 47 obese women at one year follow-up. We evaluated biochemical parameters and serum inflammatory cytokines -TNFα, IL6 and IL1β- to assess systemic status. Total superoxide production -dHe-, mitochondrial membrane potential -TMRM-, leucocyte protein expression of inflammation mediators -MCP1 and NF-kB-, antioxidant defence -GPX1-, mitochondrial regulation—PGC1α, TFAM, OXPHOS and MIEAP- and dynamics -MFN2, MNF1, OPA1, FIS1 and p-DRP1- were also determined. After RYGB, a significant reduction in superoxide and mitochondrial membrane potential was...

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Roux-en-Y Gastric Bypass Modulates AMPK, Autophagy and Inflammatory Response in Leukocytes of Obese Patients

Biomedicines, 2022

Obesity is characterized by low-grade chronic inflammation, metabolic overload, and impaired endo... more Obesity is characterized by low-grade chronic inflammation, metabolic overload, and impaired endothelial and cardiovascular function. Roux-en-Y gastric bypass (RYGB) results in amelioration of the pro-oxidant status of leukocytes and the metabolic profile. Nevertheless, little is known about the precise mechanism that drives systemic and metabolic improvements following bariatric surgery. In this cohort study, we investigated the effect of RYGB on molecular pathways involving energy homeostasis in leukocytes in 43 obese subjects one year after surgery. In addition to clinical and biochemical parameters, we determined protein expression of systemic proinflammatory cytokines by Luminex®, different markers of inflammation, endoplasmic reticulum (ER) stress, autophagy/mitophagy by western blot, and mitochondrial membrane potential by fluorescence imaging. Bariatric surgery induced an improvement in metabolic outcomes that was accompanied by a systemic drop in hsCRP, IL6, and IL1β levels...

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Does Empagliflozin Modulate Leukocyte–Endothelium Interactions, Oxidative Stress, and Inflammation in Type 2 Diabetes?

Antioxidants, 2021

Sodium-glucose co-transporter 2 inhibitors (iSGLT2) have been linked to cardiovascular risk reduc... more Sodium-glucose co-transporter 2 inhibitors (iSGLT2) have been linked to cardiovascular risk reduction in patients with type 2 diabetes (T2D). However, their underlying molecular mechanisms remain unclear. This study aimed to evaluate the effects of empagliflozin, a novel potent and selective iSGLT-2, on anthropometric and endocrine parameters, leukocyte–endothelium interactions, adhesion molecules, ROS production, and NFkB-p65 transcription factor expression. According to standard clinical protocols, sixteen T2D patients receiving 10 mg/day of empagliflozin were followed-up for 24 weeks. Anthropometric and analytical measurements were performed at baseline, 12 weeks, and 24 weeks. Interactions between polymorphonuclear leukocytes and human umbilical vein endothelial cells (HUVECs), serum levels of adhesion molecules (P-Selectin, VCAM-1 and ICAM-1) and pro-inflammatory cytokines (TNF-α, IL-1β and IL-6), mitochondrial ROS levels, antioxidant enzymes (SOD1 and GPX1), and NFkB-p65 were ...

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Effect of Roux-en-Y Bariatric Bypass Surgery on Subclinical Atherosclerosis and Oxidative Stress Markers in Leukocytes of Obese Patients: A One-Year Follow-Up Study

Antioxidants, 2020

Little is known about the mechanisms underlying the cardioprotective effect of Roux en-Y gastric ... more Little is known about the mechanisms underlying the cardioprotective effect of Roux en-Y gastric bypass (RYGB) surgery. Therefore, the aim of the present study was to investigate whether weight loss associated with RYGB improves the oxidative status of leukocytes and ameliorates subclinical atherosclerotic markers. This is an interventional study of 57 obese subjects who underwent RYGB surgery. We determined biochemical parameters and qualitative analysis of cholesterol, leukocyte and systemic oxidative stress markers —superoxide production, glutathione peroxidase 1 (GPX1), superoxide dismutase (SOD) activity and protein carbonylation—, soluble cellular adhesion molecules —sICAM-1 and sP-selectin—, myeloperoxidase (MPO) and leukocyte-endothelium cell interactions—rolling flux, velocity and adhesion. RYGB induced an improvement in metabolic parameters, including hsCRP and leukocyte count (p < 0.001, for both). This was associated with an amelioration in oxidative stress, since sup...

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Phytosterols: Nutritional Health Players in the Management of Obesity and Its Related Disorders

Antioxidants, 2020

Obesity and its related disorders, such as diabetes and cardiovascular risk, represent an emergin... more Obesity and its related disorders, such as diabetes and cardiovascular risk, represent an emerging global health issue. Even though genetic factors seem to be the primary actors in the development and progression of these diseases, dietary choices also appear to be of crucial importance. A healthy diet combined with physical activity have been shown to ameliorate glycaemic levels and insulin sensitivity, reduce body weight and the risk of chronic diseases, and contribute to an overall improvement in quality of life. Among nutrients, phytosterols have become the focus of growing attention as novel functional foods in the management of metabolic disorders. Phytosterols are natural plant compounds belonging to the triterpene family and are structurally similar to cholesterol. They are known for their cholesterol-lowering effects, anti-inflammatory and antioxidant properties, and the benefits they offer to the immune system. The present review aims to provide an overview of these bioact...

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The SGLT2 Inhibitor Empagliflozin Ameliorates the Inflammatory Profile in Type 2 Diabetic Patients and Promotes an Antioxidant Response in Leukocytes

Journal of Clinical Medicine, 2019

Sodium–glucose co-transporter 2 inhibitors (iSGLT2) have been linked to a considerable reduction ... more Sodium–glucose co-transporter 2 inhibitors (iSGLT2) have been linked to a considerable reduction in cardiovascular risk in patients with type 2 diabetes (T2D), but the precise molecular mechanisms are still elusive. We aimed to evaluate the effects of the iSGLT2 empagliflozin on systemic inflammation and its potential antioxidant properties. This is an observational, prospective follow-up study of a cohort of fifteen patients with T2D who received 10 mg/day of empagliflozin according to standard clinical care. Measures at baseline, 12 and 24 weeks were taken. Metabolic and anthropometric parameters were evaluated. Production of mitochondrial superoxide, glutathione content, and glutathione s-reductase and catalase mRNA levels were measured in leukocytes. Serum levels of myeloperoxidase, hs-CRP and IL-10 were determined. In addition to decreased body weight and reduced glucose and HbA1c levels, we observed a reduction in superoxide production in leukocytes of diabetic patients and in...

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Downregulation of miR-31 in Diabetic Nephropathy and its Relationship with Inflammation

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2018

There is a lack of reliable biological markers for the early diagnosis of diabetic nephropathy (D... more There is a lack of reliable biological markers for the early diagnosis of diabetic nephropathy (DN) during type 2 diabetes. In this pilot study we aim to assess whether miR-31 levels are modulated by the presence of DN and whether the expression of this miRNA is related to leukocyte-endothelial interactions and inflammation. Thirty-one T2D patients were enrolled in this pilot study; 18 with no diabetic complications and 13 with diabetic nephropathy. 24 non-diabetic subjects and 13 T2D patients with retinopathy (absent of other complications) were included to test the specificity of miR-31. Following anthropometric and biochemical evaluation, serum miR-31 levels were assessed by Real Time-PCR. Leukocyte-endothelial interactions were evaluated by a parallel flow chamber in vitro model. Serum TNFα, IL-6 and ICAM-1 levels were determined by XMAP-technology in a flow cytometry-based Luminex 200 instrument. Serum miR-31 levels were similar between control and T2D subjects. However, T2D pa...

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Moderate weight loss attenuates chronic endoplasmic reticulum stress and mitochondrial dysfunction in human obesity

Molecular metabolism, Jan 19, 2018

In obese patients undergoing caloric restriction, there are several potential mechanisms involved... more In obese patients undergoing caloric restriction, there are several potential mechanisms involved in the improvement of metabolic outcomes. The present study further explores whether caloric restriction can modulate endoplasmic reticulum (ER) stress and mitochondrial function, as both are known to be mechanisms underlying inflammation and insulin resistance (IR) during obesity. A total of 64 obese patients with BMI ≥35 kg/m underwent a dietary program consisting of 6 weeks of a very-low-calorie diet followed by 18 weeks of low-calorie diet. We evaluated changes in the metabolic and inflammatory markers -TNFα, hsCRP, complement component 3 (C3c), and retinol binding protein 4 (RBP4)-, in the ER stress markers and modulators -eIF2α-P, sXBP1, ATF6, JNK-P, CHOP, GRP78, and SIRT1-, and in mitochondrial function parameters -mitochondrial reactive oxygen species (mROS), glutathione peroxidase 1 (GPX1), cytosolic Ca, and mitochondrial membrane potential. The dietary intervention produced an...

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Mitochondria, the NLRP3 inflammasome and sirtuins in type 2 diabetes: new therapeutic targets

Antioxidants & redox signaling, Jan 19, 2017

Type 2 diabetes mellitus and hyperglycaemia can lead to the development of comorbidities such as ... more Type 2 diabetes mellitus and hyperglycaemia can lead to the development of comorbidities such as atherosclerosis and microvascular/macrovascular complications. Both type 2 diabetes and its complications are related to mitochondrial dysfunction and oxidative stress. Type 2 diabetes is also a chronic inflammatory condition that leads to inflammasome activation and the release of proinflammatory mediators, including interleukins 1β and 18 (IL-1β, IL-18). Moreover, sirtuins are energetic sensors that respond to metabolic load, which highlights their relevance in metabolic diseases, such as type 2 diabetes. Recent advances: Over the past decade, great progress has been made in clarifying the signalling events regulated by mitochondria, inflammasomes and sirtuins. NLRP3 is the best-characterized inflammasome, and the generation of oxidant species seems to be critical for its activation. NLRP3 inflammasome activation and altered sirtuin levels have been observed in type 2 diabetes. Critica...

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Are Mitochondrial Fusion and Fission Impaired in Leukocytes of Type 2 Diabetic Patients?

Antioxidants & Redox Signaling, 2016

Mitochondrial fusion/fission alterations have been evaluated in different tissues of type 2 diabe... more Mitochondrial fusion/fission alterations have been evaluated in different tissues of type 2 diabetic (T2D) patients. However, it is not known whether mitochondrial dynamics is disturbed in the leukocytes of T2D patients and whether glycemic control affects its regulation. Anthropometric and metabolic parameters in 91 T2D patients (48 with glycated haemoglobin [HbA1c] &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;6.5% and 43 with HbA1c&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt;6.5%) were characteristic of the disease, when compared to 78 control subjects. We observed increased ROS production in leukocytes from diabetic patients, together with a reduced mitochondrial oxygen consumption rate, especially in poorly controlled patients. Mitochondrial fusion was reduced and fission was increased in diabetic patients, and both features were accentuated in patients with poor glycemic control. Furthermore, leukocyte rolling flux rose in parallel to HbA1c levels. The induction of leukocyte-endothelial interactions in diabetic patients was related to a reduced mitochondrial fusion and higher mitochondrial fission. Our findings suggest that mitochondrial dynamics could be influenced by glycemic control in leukocytes of diabetic patients, in which there is decreased mitochondrial fusion and elevated fission related to enhanced leukocyte-endothelial interactions. These findings lead to the hypothesis that poor glycemic control during T2D may alter mitochondrial dynamics, and could eventually promote leukocyte-endothelial interactions and the onset of cardiovascular diseases.

Plos One

PLoS ONE

CONTEXT: Anorexia nervosa is a common illness among adolescents and is characterised by oxidative... more CONTEXT: Anorexia nervosa is a common illness among adolescents and is characterised by oxidative stress. OBJECTIVE: The effects of anorexia on mitochondrial function and redox state in leukocytes from anorexic subjects were evaluated. DESIGN AND SETTING: A multi-centre, cross-sectional case-control study was performed. PATIENTS: Our study population consisted of 20 anorexic patients and 20 age-matched controls, all of which were Caucasian women. MAIN OUTCOME MEASURES: Anthropometric and metabolic parameters were evaluated in the study population. To assess whether anorexia nervosa affects mitochondrial function and redox state in leukocytes of anorexic patients, we measured mitochondrial oxygen consumption, membrane potential, reactive oxygen species production, glutathione levels, mitochondrial mass, and complex I and III activity in polymorphonuclear cells. RESULTS: Mitochondrial function was impaired in the leukocytes of the anorexic patients. This was evident in a decrease in m...

662 Lipid Response to Phytosterols in a Hypercholesterolemic Population is Not Affected by Apolipoprotein e Polymorphism or Diameter of Low-Density Lipoprotein

Atherosclerosis Supplements, 2011

Consumption of both plant sterol-and stanol-enriched products reduces LDLcholesterol concentratio... more Consumption of both plant sterol-and stanol-enriched products reduces LDLcholesterol concentrations, whereas plant stanols also lower serum plant sterol concentrations. In contrast to plant stanols, plant sterols can undergo oxidation. This results in the formation of oxyphytosterols, which have been identified in the human circulation. Preliminary findings from animal studies suggest that oxyphytosterols may, like oxidation products of cholesterol, be atherogenic. Therefore, the objective of this study was to examine whether plant sterol and stanol consumption results in changed fasting serum oxyphytosterol concentrations. A randomized, double-blind, cross-over study was performed in which 46 healthy subjects (18−70 years) consumed for 4 weeks a plant sterol-enriched (3.0 g/d of plant sterols), a plant stanol-enriched (3.0 g/d of plant stanols), and a control margarine separated by wash-out periods of 4 weeks. Serum oxyphytosterol concentrations were determined in BHT-enriched plasma via GC-MS. Serum total cholesterol concentrations were reduced by 0.25 mmol/L (−4.5%) after sterol consumption and by 0.23 mmol/L (−4.2%) after stanol consumption. Plant sterol or plant stanol ester consumption did not change 7a-OHsitosterol, 7a-OH-campesterol, 7b-OH-sitosterol, 7-keto-sitosterol and 7-ketocampesterol concentrations. On the other hand, plant stanol consumption reduced especially 7b-OH-campesterol by nearly 10 ng/mmol cholesterol, (~16%; p < 0.05) compared with plant sterol consumption and by more than 9 ng/mmol cholesterol (~15%; p < 0.05) compared with controls. These results indicate that whereas daily consumption of a plant sterol-enriched margarine does not increase concentrations of oxidative compounds, plant stanol consumption can reduce the concentration of in particular the oxidative plant sterol metabolite 7b-OH-campesterol.

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The Mitochondria-Targeted Antioxidant MitoQ Modulates Mitochondrial Function and Endoplasmic Reticulum Stress in Pancreatic β Cells Exposed to Hyperglycaemia

Cellular Physiology and Biochemistry, Feb 28, 2019

This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 I... more

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Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Diabetes

Current Pharmaceutical Design, May 5, 2016

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Oxidative Stress, Endothelial Dysfunction and Atherosclerosis

Current Pharmaceutical Design, Sep 1, 2009