Antioxidants

Editorial

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5 pages, 204 KiB

Open AccessEditorial

Redox Regulation of Metabolic Syndrome: From Biochemical Mechanisms to Nutritional Interventions

by Mario Allegra

Antioxidants 2021, 10(5), 638; https://doi.org/10.3390/antiox10050638 - 22 Apr 2021

Viewed by 1767

Abstract

According to its “harmonized” definition, metabolic syndrome (MetS) is described as a cluster of metabolic factors that increases the risk of cardiovascular diseases, diabetes (DM) and associated morbidities such as dementia [...] Full article

(This article belongs to the Special Issue Redox Regulation of Metabolic Syndrome: From Biochemical Mechanisms to Nutritional Interventions)

Research

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18 pages, 1597 KiB

Open AccessArticle

Blunted Reducing Power Generation in Erythrocytes Contributes to Oxidative Stress in Prepubertal Obese Children with Insulin Resistance

by Álvaro González-Domínguez, Francisco Visiedo, Jesus Domínguez-Riscart, Beatriz Ruiz-Mateos, Ana Saez-Benito, Alfonso M. Lechuga-Sancho and Rosa María Mateos

Antioxidants 2021, 10(2), 244; https://doi.org/10.3390/antiox10020244 - 5 Feb 2021

Cited by 17 | Viewed by 4016

Abstract

Childhood obesity, and specifically its metabolic complications, are related to deficient antioxidant capacity and oxidative stress. Erythrocytes are constantly exposed to multiple sources of oxidative stress; hence, they are equipped with powerful antioxidant mechanisms requiring permanent reducing power generation and turnover. Glucose-6-phosphate dehydrogenase [...] Read more.

Childhood obesity, and specifically its metabolic complications, are related to deficient antioxidant capacity and oxidative stress. Erythrocytes are constantly exposed to multiple sources of oxidative stress; hence, they are equipped with powerful antioxidant mechanisms requiring permanent reducing power generation and turnover. Glucose-6-phosphate dehydrogenase (G6PDH) and 6-phosphogluconate dehydrogenase (6PGDH) are two key enzymes on the pentose phosphate pathway. Both enzymes supply reducing power by generating NADPH, which is essential for maintaining the redox balance within the cell and the activity of other antioxidant enzymes. We hypothesized that obese children with insulin resistance would exhibit blunted G6PDH and 6PGDH activities, contributing to their erythrocytes’ redox status imbalances. We studied 15 control and 24 obese prepubertal children, 12 of whom were insulin-resistant according to an oral glucose tolerance test (OGTT). We analyzed erythroid malondialdehyde (MDA) and carbonyl group levels as oxidative stress markers. NADP+/NADPH and GSH/GSSG were measured to determine redox status, and NADPH production by both G6PDH and 6PGDH was assayed spectrophotometrically to characterize pentose phosphate pathway activity. Finally, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and glutathione reductase (GR) activities were also assessed. As expected, MDA and carbonyl groups levels were higher at baseline and along the OGTT in insulin-resistant children. Both redox indicators showed an imbalance in favor of the oxidized forms along the OGTT in the insulin-resistant obese group. Additionally, the NADPH synthesis, as well as GR activity, were decreased. H₂O₂ removing enzyme activities were depleted at baseline in both obese groups, although after sugar intake only metabolically healthy obese participants were able to maintain their catalase activity. No change was detected in SOD activity between groups. Our results show that obese children with insulin resistance present higher levels of oxidative damage, blunted capacity to generate reducing power, and hampered function of key NADPH-dependent antioxidant enzymes. Full article

(This article belongs to the Special Issue Redox Regulation of Metabolic Syndrome: From Biochemical Mechanisms to Nutritional Interventions)

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18 pages, 2987 KiB

Open AccessArticle

Resveratrol-Elicited PKC Inhibition Counteracts NOX-Mediated Endothelial to Mesenchymal Transition in Human Retinal Endothelial Cells Exposed to High Glucose

by Roberta Giordo, Gheyath K. Nasrallah, Anna Maria Posadino, Francesco Galimi, Giampiero Capobianco, Ali Hussein Eid and Gianfranco Pintus

Antioxidants 2021, 10(2), 224; https://doi.org/10.3390/antiox10020224 - 2 Feb 2021

Cited by 49 | Viewed by 3353

Abstract

Diabetes-associated long-term hyperglycaemia leads to oxidative stress-mediated fibrosis in different tissues and organs. Endothelial-to-mesenchymal-transition (EndMT) appears to play a role in diabetes-associated fibrotic conditions. Here, we investigate whether EndMT is implicated in the diabetic retinopathy fibrotic process and evaluate the possibility that resveratrol [...] Read more.

Diabetes-associated long-term hyperglycaemia leads to oxidative stress-mediated fibrosis in different tissues and organs. Endothelial-to-mesenchymal-transition (EndMT) appears to play a role in diabetes-associated fibrotic conditions. Here, we investigate whether EndMT is implicated in the diabetic retinopathy fibrotic process and evaluate the possibility that resveratrol could counteract EndMT by inhibiting high glucose (HG)-induced increases in ROS. Primary Human Retinal Endothelial Cells (HRECs) were either pre-treated for 24 h with 1 µM resveratrol or left untreated, then glucose (30 mM) was applied at 3-day intervals for 10 days. qRT-PCR and ELISA were used to detect mRNA or protein expression of endothelial markers (CD31, CDH5, vWF) or mesenchymal markers (VIM, αSMA and collagen I), respectively. Intracellular ROS levels were measured with carboxy-DCFDA, while NOX-associated ROS levels were evaluated using the NADPH-specific redox biosensor p47-roGFP. Treatment of HRECs with HG increased intracellular ROS levels and promoted phenotype shifting towards EndMT, evidenced by decreased expression of endothelial markers concomitant with increased expression of mesenchymal ones. HG-induced EndMT appears to be mediated by NADPH-associated ROS generation as pre-treatment of HRECs with resveratrol or the NADPH inhibitor, diphenyleneiodonium chloride (DPI), attenuated ROS production and EndMT transition, suggesting that the effect of resveratrol on HG-induced ROS occurs via down-regulation of NADPH oxidase. It is worth noting that resveratrol or Chelerythrine, a Protein kinase C (PKC) inhibitor, reduce ROS and EndMT in HG-exposed cells, suggesting that NADPH activation occurs via a PKC-dependent mechanism. Taken together, our results provide the basis for a resveratrol-based potential protective therapy to prevent diabetic-associated complications. Full article

(This article belongs to the Special Issue Redox Regulation of Metabolic Syndrome: From Biochemical Mechanisms to Nutritional Interventions)

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17 pages, 1708 KiB

Open AccessArticle

S-Nitrosoglutathione Reverts Dietary Sucrose-Induced Insulin Resistance

by Inês Sousa-Lima, Ana B. Fernandes, Rita S. Patarrão, Young-Bum Kim and M. Paula Macedo

Antioxidants 2020, 9(9), 870; https://doi.org/10.3390/antiox9090870 - 15 Sep 2020

Cited by 4 | Viewed by 3005

Abstract

The liver is a fundamental organ to ensure whole-body homeostasis, allowing for a proper increase in insulin sensitivity from the fast to the postprandial status. Hepatic regulation of glucose metabolism is crucial and has been shown to be modulated by glutathione (GSH) and [...] Read more.

The liver is a fundamental organ to ensure whole-body homeostasis, allowing for a proper increase in insulin sensitivity from the fast to the postprandial status. Hepatic regulation of glucose metabolism is crucial and has been shown to be modulated by glutathione (GSH) and nitric oxide (NO). However, knowledge of the metabolic action of GSH and NO in glucose homeostasis remains incomplete. The current study was designed to test the hypothesis that treatment with S-nitrosoglutathione is sufficient to revert insulin resistance induced by a high-sucrose diet. Male Wistar rats were divided in a control or high-sucrose group. Insulin sensitivity was determined: (i) in the fast state; (ii) after a standardized test meal; (iii) after GSH + NO; and after (iv) S-nitrosoglutathione (GSNO) administration. The fasting glucose level was not different between the control and high-sucrose group. In the liver, the high-sucrose model shows increased NO and unchanged GSH levels. In control animals, insulin sensitivity increased after a meal or administration of GSH+NO/GSNO, but this was abrogated by sucrose feeding. GSNO was able to revert insulin resistance induced by sucrose feeding, in a dose-dependent manner, suggesting that they have an insulin-sensitizing effect in vivo. These effects are associated with an increased insulin receptor and Akt phosphorylation in muscle cells. Our findings demonstrate that GSNO promotes insulin sensitivity in a sucrose-induced insulin-resistant animal model and further implicates that this antioxidant molecule may act as a potential pharmacological tool for the treatment of insulin resistance in obesity and type 2 diabetes. Full article

(This article belongs to the Special Issue Redox Regulation of Metabolic Syndrome: From Biochemical Mechanisms to Nutritional Interventions)

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17 pages, 2405 KiB

Open AccessArticle

Systemic Insulin Resistance and Metabolic Perturbations in Chow Fed Inducible Nitric Oxide Synthase Knockout Male Mice: Partial Reversal by Nitrite Supplementation

by Hobby Aggarwal, Priya Pathak, Pragati Singh, Jiaur R. Gayen, Kumaravelu Jagavelu and Madhu Dikshit

Antioxidants 2020, 9(8), 736; https://doi.org/10.3390/antiox9080736 - 12 Aug 2020

Cited by 12 | Viewed by 3937

Abstract

iNOS, an important mediator of inflammation, has emerged as an important metabolic regulator. There are conflicting observations on the incidence of insulin resistance (IR) due to hyperglycemia/dyslipidemia in iNOS^−/− mice. There are reports that high fat diet (HFD) fed mice exhibited no [...] Read more.

iNOS, an important mediator of inflammation, has emerged as an important metabolic regulator. There are conflicting observations on the incidence of insulin resistance (IR) due to hyperglycemia/dyslipidemia in iNOS^−/− mice. There are reports that high fat diet (HFD) fed mice exhibited no change, protection, or enhanced susceptibility to IR. Similar observations were also reported for low fat diet (LFD) fed KO mice. In the present study chow fed iNOS^−/− mice were examined for the incidence of IR, and metabolic perturbations, and also for the effect of sodium nitrite supplementation (50 mg/L). In IR-iNOS^−/− mice, we observed significantly higher body weight, BMI, adiposity, blood glucose, HOMA-IR, serum/tissue lipids, glucose intolerance, enhanced gluconeogenesis, and disrupted insulin signaling. Expression of genes involved in hepatic and adipose tissue lipid uptake, synthesis, oxidation, and gluconeogenesis was upregulated with concomitant downregulation of genes for hepatic lipid excretion. Nitrite supplementation restored NO levels, significantly improved systemic IR, glucose tolerance, and also reduced lipid accumulation by rescuing hepatic insulin sensitivity, glucose, and lipid homeostasis. Obesity, gluconeogenesis, and adipose tissue insulin signaling were only partially reversed in nitrite supplemented iNOS^−/− mice. Our results thus demonstrate that nitrite supplementation to iNOS^−/− mice improves insulin sensitivity and metabolic homeostasis, thus further highlighting the metabolic role of iNOS. Full article

(This article belongs to the Special Issue Redox Regulation of Metabolic Syndrome: From Biochemical Mechanisms to Nutritional Interventions)

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17 pages, 1341 KiB

Open AccessArticle

The Impact of Sugar-Sweetened Beverage Consumption on the Liver: A Proteomics-Based Analysis

by Janina Benade, Lucien Sher, Sheneez De Klerk, Gaurang Deshpande, Dirk Bester, Jeanine L. Marnewick, Gary Sieck, Ismail Laher and M. Faadiel Essop

Antioxidants 2020, 9(7), 569; https://doi.org/10.3390/antiox9070569 - 1 Jul 2020

Cited by 5 | Viewed by 3888

Abstract

Cardiometabolic complications such as the metabolic syndrome and Type 2 Diabetes Mellitus (T2DM) are major causes of global morbidity and mortality. As sugar-sweetened beverages (SSBs) are implicated in this process, this study aimed to obtain greater mechanistic insights. Male Wistar rats (~200 g) [...] Read more.

Cardiometabolic complications such as the metabolic syndrome and Type 2 Diabetes Mellitus (T2DM) are major causes of global morbidity and mortality. As sugar-sweetened beverages (SSBs) are implicated in this process, this study aimed to obtain greater mechanistic insights. Male Wistar rats (~200 g) were gavaged with a local SSB every day for a period of six months while the control group was gavaged with an iso-volumetric amount of water. Experimental dosages were calculated according to the surface area-to-volume ratio and were equivalent to 125 mL/day (in human terms). A proteomic analysis was performed on isolated liver samples and thereafter, markers of endoplasmic reticulum (ER) stress, antioxidant/oxidant capacity, calcium regulation, and mitochondrial functionality were assessed. These data show that SSB consumption resulted in (a) the induction of mild hepatic ER stress; (b) altered hepatic mitochondrial dynamics; and (c) perturbed calcium handling across mitochondria-associated ER membranes. Despite significant changes in markers of ER stress, the antioxidant response and calcium handling (proteomics data), the liver is able to initiate adaptive responses to counteract such stressors. However, the mitochondrial data showed increased fission and decreased fusion that may put the organism at risk for developing insulin resistance and T2DM in the longer term. Full article

(This article belongs to the Special Issue Redox Regulation of Metabolic Syndrome: From Biochemical Mechanisms to Nutritional Interventions)

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10 pages, 238 KiB

Open AccessArticle

Risk Associated with the LEPR rs8179183 GG Genotype in a Female Korean Population with Obesity

by Kyunghye Jang, Gurum Shin, Hye Jin Yoo, Jong Ho Lee and Minjoo Kim

Antioxidants 2020, 9(6), 497; https://doi.org/10.3390/antiox9060497 - 6 Jun 2020

Cited by 1 | Viewed by 2719

Abstract

The difference between metabolically healthy obesity (MHO) and metabolically unhealthy obesity (MUO) phenotypes might be partly attributable to genetic traits modulating body fat distribution and other obesity-related metabolic traits, specifically with regard to LEPR rs8179183 in Korean women with obesity. A total of [...] Read more.

The difference between metabolically healthy obesity (MHO) and metabolically unhealthy obesity (MUO) phenotypes might be partly attributable to genetic traits modulating body fat distribution and other obesity-related metabolic traits, specifically with regard to LEPR rs8179183 in Korean women with obesity. A total of 177 females with obesity participated in the study and were grouped by genotype (GC or GG) and metabolic health status (MHO and MUO). Between the MHO and MUO groups, significant differences were found in waist circumference, waist-to-hip ratio, lipid profiles, glucose-related markers, biomarkers of liver health, adiponectin, oxidative stress markers, whole fat area (WFA), and subcutaneous fat area (SFA) at the level of the L1 vertebra, and WFA and visceral fat area (VFA) at the level of the L4 vertebra. Lipid profiles, glucose-related markers, adipokines, oxidative stress markers, and WFA and VFA at the L4 level were significantly different between the GC and GG genotypes. Notably, the individuals with the MUO phenotype and the GG genotype had the least favorable values of glucose-related markers, lipid profiles, adipokines, oxidative stress markers, and regional fat distribution. These observations suggest that the development of obesity-related metabolic traits is highly associated not only with the rs8179183 genotype but also with metabolic status in Korean females with obesity. Full article

(This article belongs to the Special Issue Redox Regulation of Metabolic Syndrome: From Biochemical Mechanisms to Nutritional Interventions)

25 pages, 3795 KiB

Open AccessArticle

Supplementation with a Carob (Ceratonia siliqua L.) Fruit Extract Attenuates the Cardiometabolic Alterations Associated with Metabolic Syndrome in Mice

by María de la Fuente-Fernández, Daniel González-Hedström, Sara Amor, Antonio Tejera-Muñoz, Nuria Fernández, Luis Monge, Paula Almodóvar, Laura Andrés-Delgado, Luis Santamaría, Marin Prodanov, Antonio Manuel Inarejos-García, Angel Luis García-Villalón and Miriam Granado

Antioxidants 2020, 9(4), 339; https://doi.org/10.3390/antiox9040339 - 21 Apr 2020

Cited by 20 | Viewed by 6571

Abstract

The incidence of metabolic syndrome (MetS) is increasing worldwide which makes necessary the finding of new strategies to treat and/or prevent it. The aim of this study was to analyze the possible beneficial effects of a carob fruit extract (CSAT+^®) on [...] Read more.

The incidence of metabolic syndrome (MetS) is increasing worldwide which makes necessary the finding of new strategies to treat and/or prevent it. The aim of this study was to analyze the possible beneficial effects of a carob fruit extract (CSAT+^®) on the cardiometabolic alterations associated with MetS in mice. 16-week-old C57BL/6J male mice were fed for 26 weeks either with a standard diet (chow) or with a diet rich in fats and sugars (HFHS), supplemented or not with 4.8% of CSAT+^®. CSAT+^® supplementation reduced blood glucose, Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) and circulating levels of total cholesterol, low-density lipoprotein (LDL) cholesterol (LDL-c), insulin, and interleukin-6 (IL-6). In adipose tissue and skeletal muscle, CSAT+^® prevented MetS-induced insulin resistance, reduced macrophage infiltration and the expression of pro-inflammatory markers, and up-regulated the mRNA levels of antioxidant markers. Supplementation with CSAT+^® prevented MetS-induced hypertension and decreased the vascular response of aortic rings to angiotensin II (AngII). Moreover, treatment with CSAT+^® attenuated endothelial dysfunction and increased vascular sensitivity to insulin. In the heart, CSAT+^® supplementation reduced cardiomyocyte apoptosis and prevented ischemia-reperfusion-induced decrease in cardiac contractility. The beneficial effects at the cardiovascular level were associated with a lower expression of pro-inflammatory and pro-oxidant markers in aortic and cardiac tissues. Full article

(This article belongs to the Special Issue Redox Regulation of Metabolic Syndrome: From Biochemical Mechanisms to Nutritional Interventions)

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19 pages, 2128 KiB

Open AccessArticle

Metabolomics Elucidates Dose-Dependent Molecular Beneficial Effects of Hesperidin Supplementation in Rats Fed an Obesogenic Diet

by Maria Guirro, Andreu Gual-Grau, Albert Gibert-Ramos, Juan Maria Alcaide-Hidalgo, Núria Canela, Lluís Arola and Jordi Mayneris-Perxachs

Antioxidants 2020, 9(1), 79; https://doi.org/10.3390/antiox9010079 - 16 Jan 2020

Cited by 25 | Viewed by 4718

Abstract

Metabolic syndrome (MetS) is a global epidemic concern. Polyphenols are proposed as good candidates for its prevention, although their mechanisms are not fully understood. The gut microbiota seems to play a key role in polyphenol beneficial effects. Here, we assessed the effects of [...] Read more.

Metabolic syndrome (MetS) is a global epidemic concern. Polyphenols are proposed as good candidates for its prevention, although their mechanisms are not fully understood. The gut microbiota seems to play a key role in polyphenol beneficial effects. Here, we assessed the effects of the citrus polyphenol hesperidin combining an untargeted metabolomics approach, which has an inherent potential to elucidate the host-microbiome interplay, with extensive anthropometric and biochemical characterizations and integrating metabolomics results with our previous 16S rRNA bacterial sequencing data. The rats were fed either a standard or an obesogenic cafeteria diet (CAF) for 17 weeks. After nine weeks, rats were supplemented with vehicle; low- (H1), or high- (H2) hesperidin doses. CAF animals developed MetS features. Hesperidin supplementation in CAF rats decreased the total cholesterol, LDL-C, and free fatty acids. The highest hesperidin dose also ameliorated blood pressure, insulin sensitivity, and decreased markers of arterial stiffness and inflammation. Metabolomics revealed an improvement of the lipidomic profile, decreases in circulating amino acids, and lower excretions of inflammation- and oxidative stress-related metabolites. Bacteroidaceae increases in the CAF-H2 group paralleled higher excretions of microbial-derived metabolites. Overall, our results provide detailed insights into the molecular effects of hesperidin on MetS and suggest that it is a promising prebiotic for the treatment of MetS and related conditions. Full article

(This article belongs to the Special Issue Redox Regulation of Metabolic Syndrome: From Biochemical Mechanisms to Nutritional Interventions)

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13 pages, 2911 KiB

Open AccessArticle

Extra Virgin Olive Oil and Nigella sativa Oil Produced in Central Italy: A Comparison of the Nutrigenomic Effects of Two Mediterranean Oils in a Low-Grade Inflammation Model

by Laura Bordoni, Donatella Fedeli, Dennis Fiorini and Rosita Gabbianelli

Antioxidants 2020, 9(1), 20; https://doi.org/10.3390/antiox9010020 - 24 Dec 2019

Cited by 19 | Viewed by 5108

Abstract

Extra virgin olive (EVO) oil and Nigella sativa (NG) oil are two well-known Mediterranean foods whose consumption has been associated with beneficial effects on human health. This study investigates the nutrigenomic properties of two high quality EVO and NG oils in an in [...] Read more.

Extra virgin olive (EVO) oil and Nigella sativa (NG) oil are two well-known Mediterranean foods whose consumption has been associated with beneficial effects on human health. This study investigates the nutrigenomic properties of two high quality EVO and NG oils in an in vitro model of low-grade inflammation of human macrophages (THP-1 cells). The aim was to assess whether these healthy foods could modulate inflammation through antioxidant and epigenetic mechanisms. When THP-1 cells were co-exposed to both lipopolysaccharides (LPS)-induced inflammation and oils, both EVO and NG oils displayed anti-inflammatory activity. Both oils were able to restore normal expression levels of DNMT3A and HDAC1 (but not DNMT3B), which were altered under inflammatory conditions. Moreover, EVO oil was able to prevent the increase in TET2 expression and reduce global DNA methylation that were measured in inflamed cells. Due to its antioxidant properties, EVO oil was particularly efficient in restoring normal levels of membrane fluidity, which, on the contrary, were reduced in the presence of inflammation. In conclusion, these data support the hypothesis that these Mediterranean oils could play a major role in the modulation of low-grade inflammation and metabolic syndrome prevention. However, NS oil seems to be more efficient in the control of proinflammatory cytokines, whereas EVO oil better helps to counteract redox imbalance. Further studies that elucidate the nutrigenomic properties of local produce might help to promote regional the production and consumption of high-quality food, which could also help the population to maintain and promote health. Full article

(This article belongs to the Special Issue Redox Regulation of Metabolic Syndrome: From Biochemical Mechanisms to Nutritional Interventions)

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13 pages, 1517 KiB

Open AccessArticle

Effects of Very Low Calorie Ketogenic Diet on the Orexinergic System, Visceral Adipose Tissue, and ROS Production

by Anna Valenzano, Rita Polito, Valentina Trimigno, Antonella Di Palma, Fiorenzo Moscatelli, Gaetano Corso, Francesco Sessa, Monica Salerno, Angelo Montana, Nunzio Di Nunno, Marinella Astuto, Aurora Daniele, Marco Carotenuto, Giovanni Messina, Giuseppe Cibelli and Vincenzo Monda

Antioxidants 2019, 8(12), 643; https://doi.org/10.3390/antiox8120643 - 13 Dec 2019

Cited by 63 | Viewed by 6653

Abstract

Background: Caloric restriction is a valid strategy to reduce the visceral adipose tissue (VAT) content in obese persons. Hypocretin-1 (orexin-A) is a neuropeptide synthesized in the lateral hypothalamus that strongly modulates food intake, thus influencing adipose tissue accumulation. Therapeutic diets in obesity treatment [...] Read more.

Background: Caloric restriction is a valid strategy to reduce the visceral adipose tissue (VAT) content in obese persons. Hypocretin-1 (orexin-A) is a neuropeptide synthesized in the lateral hypothalamus that strongly modulates food intake, thus influencing adipose tissue accumulation. Therapeutic diets in obesity treatment may combine the advantages of caloric restriction and dietary ketosis. The current study aimed to evaluate the effect of a very low calorie ketogenic diet (VLCKD) in a population of obese patients. Methods: Adiposity parameters and orexin-A serum profiling were quantified over an 8 week period. The effect of the VLCKD on reactive oxygen species (ROS) production and cell viability was evaluated, in vitro, by culturing Hep-G2 cells in the presence of VLCKD sera. Results: Dietary intervention induced significant effects on body weight, adiposity, and blood chemistry parameters. Moreover, a selective reduction in VAT was measured by dual-energy X-ray absorptiometry. Orexin-A levels significantly increased after dietary treatment. Hep-G2 cell viability was not affected after 24, 48, and 72 h incubation with patients’ sera, before and after the VLCKD. In the same model system, ROS production was not significantly influenced by dietary treatment. Conclusion: The VLCKD exerts a positive effect on VAT decrease, ameliorating adiposity and blood chemistry parameters. Furthermore, short-term mild dietary ketosis does not appear to have a cytotoxic effect, nor does it represent a factor capable of increasing oxidative stress. Finally, to the best of our knowledge, this is the first study that shows an effect of the VLCKD upon the orexinergic system, supporting the usefulness of such a therapeutic intervention in promoting obesity reduction in the individual burden of this disease. Full article

(This article belongs to the Special Issue Redox Regulation of Metabolic Syndrome: From Biochemical Mechanisms to Nutritional Interventions)

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Review

Jump to: Editorial, Research

25 pages, 1818 KiB

Open AccessReview

Mechanisms of Non-Alcoholic Fatty Liver Disease in the Metabolic Syndrome. A Narrative Review

by Luca Rinaldi, Pia Clara Pafundi, Raffaele Galiero, Alfredo Caturano, Maria Vittoria Morone, Chiara Silvestri, Mauro Giordano, Teresa Salvatore and Ferdinando Carlo Sasso

Antioxidants 2021, 10(2), 270; https://doi.org/10.3390/antiox10020270 - 10 Feb 2021

Cited by 124 | Viewed by 12390

Abstract

Non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome (MS) are two different entities sharing common clinical and physio-pathological features, with insulin resistance (IR) as the most relevant. Large evidence leads to consider it as a risk factor for cardiovascular disease, regardless of age, [...] Read more.

Non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome (MS) are two different entities sharing common clinical and physio-pathological features, with insulin resistance (IR) as the most relevant. Large evidence leads to consider it as a risk factor for cardiovascular disease, regardless of age, sex, smoking habit, cholesterolemia, and other elements of MS. Therapeutic strategies remain still unclear, but lifestyle modifications (diet, physical exercise, and weight loss) determine an improvement in IR, MS, and both clinical and histologic liver picture. NAFLD and IR are bidirectionally correlated and, consequently, the development of pre-diabetes and diabetes is the most direct consequence at the extrahepatic level. In turn, type 2 diabetes is a well-known risk factor for multiorgan damage, including an involvement of cardiovascular system, kidney and peripheral nervous system. The increased MS incidence worldwide, above all due to changes in diet and lifestyle, is associated with an equally significant increase in NAFLD, with a subsequent rise in both morbidity and mortality due to both metabolic, hepatic and cardiovascular diseases. Therefore, the slowdown in the increase of the “bad company” constituted by MS and NAFLD, with all the consequent direct and indirect costs, represents one of the main challenges for the National Health Systems. Full article

(This article belongs to the Special Issue Redox Regulation of Metabolic Syndrome: From Biochemical Mechanisms to Nutritional Interventions)

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13 pages, 4322 KiB

Open AccessReview

Suicidal Erythrocyte Death in Metabolic Syndrome

by Ignazio Restivo, Alessandro Attanzio, Luisa Tesoriere and Mario Allegra

Antioxidants 2021, 10(2), 154; https://doi.org/10.3390/antiox10020154 - 21 Jan 2021

Cited by 21 | Viewed by 3593

Abstract

Eryptosis is a coordinated, programmed cell death culminating with the disposal of cells without disruption of the cell membrane and the release of endocellular oxidative and pro-inflammatory milieu. While providing a convenient form of death for erythrocytes, dysregulated eryptosis may result in a [...] Read more.

Eryptosis is a coordinated, programmed cell death culminating with the disposal of cells without disruption of the cell membrane and the release of endocellular oxidative and pro-inflammatory milieu. While providing a convenient form of death for erythrocytes, dysregulated eryptosis may result in a series of detrimental and harmful pathological consequences highly related to the endothelial dysfunction (ED). Metabolic syndrome (MetS) is described as a cluster of cardiometabolic factors (hyperglycemia, dyslipidemia, hypertension and obesity) that increases the risk of cardiovascular complications such as those related to diabetes and atherosclerosis. In the light of the crucial role exerted by the eryptotic process in the ED, the focus of the present review is to report and discuss the involvement of eryptosis within MetS, where vascular complications are utterly relevant. Current knowledge on the mechanisms leading to eryptosis in MetS-related conditions (hyperglycemia, dyslipidemia, hypertension and obesity) will be analyzed. Moreover, clinical evidence supporting or proposing a role for eryptosis in the ED, associated to MetS cardiovascular complications, will be discussed. Full article

(This article belongs to the Special Issue Redox Regulation of Metabolic Syndrome: From Biochemical Mechanisms to Nutritional Interventions)

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31 pages, 2179 KiB

Open AccessReview

Magnesium, Oxidative Stress, Inflammation, and Cardiovascular Disease

by Man Liu and Samuel C. Dudley, Jr.

Antioxidants 2020, 9(10), 907; https://doi.org/10.3390/antiox9100907 - 23 Sep 2020

Cited by 88 | Viewed by 20184

Abstract

Hypomagnesemia is commonly observed in heart failure, diabetes mellitus, hypertension, and cardiovascular diseases. Low serum magnesium (Mg) is a predictor for cardiovascular and all-cause mortality and treating Mg deficiency may help prevent cardiovascular disease. In this review, we discuss the possible mechanisms by [...] Read more.

Hypomagnesemia is commonly observed in heart failure, diabetes mellitus, hypertension, and cardiovascular diseases. Low serum magnesium (Mg) is a predictor for cardiovascular and all-cause mortality and treating Mg deficiency may help prevent cardiovascular disease. In this review, we discuss the possible mechanisms by which Mg deficiency plays detrimental roles in cardiovascular diseases and review the results of clinical trials of Mg supplementation for heart failure, arrhythmias and other cardiovascular diseases. Full article

(This article belongs to the Special Issue Redox Regulation of Metabolic Syndrome: From Biochemical Mechanisms to Nutritional Interventions)

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16 pages, 428 KiB

Open AccessReview

Natural Compounds as Beneficial Antioxidant Agents in Neurodegenerative Disorders: A Focus on Alzheimer’s Disease

by Antonella Amato, Simona Terzo and Flavia Mulè

Antioxidants 2019, 8(12), 608; https://doi.org/10.3390/antiox8120608 - 30 Nov 2019

Cited by 78 | Viewed by 6000

Abstract

The positive role of nutrition in chronic neurodegenerative diseases (NDs) suggests that dietary interventions represent helpful tools for preventing NDs. In particular, diets enriched with natural compounds have become an increasingly attractive, non-invasive, and inexpensive option to support a healthy brain and to [...] Read more.

The positive role of nutrition in chronic neurodegenerative diseases (NDs) suggests that dietary interventions represent helpful tools for preventing NDs. In particular, diets enriched with natural compounds have become an increasingly attractive, non-invasive, and inexpensive option to support a healthy brain and to potentially treat NDs. Bioactive compounds found in vegetables or microalgae possess special properties able to counteract oxidative stress, which is involved as a triggering factor in neurodegeneration. Here, we briefly review the relevant experimental data on curcuminoids, silymarin, chlorogenic acid, and compounds derived from the microalga Aphanizomenon flos aquae (AFA) which have been demonstrated to possess encouraging beneficial effects on neurodegeneration, in particular on Alzheimer’s disease models. Full article

(This article belongs to the Special Issue Redox Regulation of Metabolic Syndrome: From Biochemical Mechanisms to Nutritional Interventions)

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