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Oxidative Stress and Inflammation in Metabolic Syndrome

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A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 29861

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Dr. Miguel D. Ferrer

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Research Group on Community Nutrition and Oxidative Stress, Science Laboratory of Physical Activity, Department of Fundamental Biology and Health Sciences, University of Balearic Islands, 07122 Palma de Mallorca, Spain
Interests: oxidative stress; inflammation; nitric oxide; vascular calcification; exercise; metabolic syndrome
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Antoni Pons

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Guest Editor

1. Research Group in Community Nutrition and Oxidative Stress, University of the Balearic Islands-IUNICS, 07122 Palma, Spain
2. Health Research Institute of Balearic Islands (IdISBa), 07120 Palma, Spain
3. CIBER Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III (ISCIII), 28029 Madrid, Spain
Interests: oxidative stress; inflammation; nitric oxide; oxylipins; exercise; metabolic syndrome;
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolic syndrome (MS) is a widespread pathologic state that manifests as multiple interrelated diseases of metabolic origin affecting the entire body, including visceral obesity, dyslipidemia, hypertension, glucose intolerance, insulin resistance, type 2 diabetes, and peripheral vascular disease. Although the causes of MS are largely dietary in origin, the consequences of its metabolic disruption cannot be solely attributed to insulin resistance, the more direct result of dietary factors, because chronic inflammation and oxidative stress also contribute to the pathologic status derived of MS. Systemic low-grade inflammation is a common feature of MS and is believed to promote disease progression. Reactive oxygen species play a direct role in adipogenesis, and oxidative stress modulates the factors involved in MS pathologies. Therefore, modulating inflammation and oxidative stress is a commonly explored strategy to prevent MS-associated comorbidities. This Special Issue aims to cover the role of inflammation and oxidative stress in the pathogenesis of MS and any therapeutic, dietary, or lifestyle strategy aiming to control or reverse these situations of chronic low-grade inflammation and oxidative stress in MS patients. To reach this goal, in vitro, animal, and human studies are welcomed.

Dr. Miguel D. Ferrer
Dr. Antoni Pons
Guest Editors

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Keywords

antioxidants
clinical trials
diabetes
inflammation
metabolic syndrome
nitric oxide
obesity
oxidative stress
reactive oxygen species

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Research

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16 pages, 4729 KiB

Open AccessArticle

Toward Ameliorating Insulin Resistance: Targeting a Novel PAK1 Signaling Pathway Required for Skeletal Muscle Mitochondrial Function

by Rekha Balakrishnan, Pablo A. Garcia, Rajakrishnan Veluthakal, Janice M. Huss, Joseph M. Hoolachan and Debbie C. Thurmond

Antioxidants 2023, 12(9), 1658; https://doi.org/10.3390/antiox12091658 - 22 Aug 2023

Cited by 2 | Viewed by 2546

Abstract

The p21-activated kinase 1 (PAK1) is required for insulin-stimulated glucose uptake in skeletal muscle cells. However, whether PAK1 regulates skeletal muscle mitochondrial function, which is a central determinant of insulin sensitivity, is unknown. Here, the effect of modulating PAK1 levels (knockdown via siRNA, overexpression via adenoviral transduction, and/or inhibition of activation via IPA3) on mitochondrial function was assessed in normal and/or insulin-resistant rat L6.GLUT4myc and human muscle (LHCN-M2) myotubes. Human type 2 diabetes (T2D) and non-diabetic (ND) skeletal muscle samples were also used for validation of the identified signaling elements. PAK1 depletion in myotubes decreased mitochondrial copy number, respiration, altered mitochondrial structure, downregulated PGC1α (a core regulator of mitochondrial biogenesis and oxidative metabolism) and PGC1α activators, p38 mitogen-activated protein kinase (p38MAPK) and activating transcription factor 2 (ATF2). PAK1 enrichment in insulin-resistant myotubes improved mitochondrial function and rescued PGC1α expression levels. Activated PAK1 was localized to the cytoplasm, and PAK1 enrichment concurrent with p38MAPK inhibition did not increase PGC1α levels. PAK1 inhibition and enrichment also modified nuclear phosphorylated-ATF2 levels. T2D human samples showed a deficit for PGC1α, and PAK1 depletion in LHCN-M2 cells led to reduced mitochondrial respiration. Overall, the results suggest that PAK1 regulates muscle mitochondrial function upstream of the p38MAPK/ATF2/PGC1α-axis pathway. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Metabolic Syndrome)

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19 pages, 754 KiB

Open AccessArticle

Association of Inflammatory and Oxidative Status Markers with Metabolic Syndrome and Its Components in 40-to-45-Year-Old Females: A Cross-Sectional Study

by Katarína Šebeková, Marta Staruchová, Csilla Mišľanová, Aurélia Líšková, Mira Horváthová, Jana Tulinská, Miroslava Lehotská Mikušová, Michaela Szabová, Radana Gurecká, Ivana Koborová, Melinda Csongová, Tamás Tábi, Éva Szökö and Katarína Volkovová

Antioxidants 2023, 12(6), 1221; https://doi.org/10.3390/antiox12061221 - 5 Jun 2023

Cited by 2 | Viewed by 2514

Abstract

Oxidative stress and sterile inflammation play roles in the induction and maintenance of metabolic syndrome (MetS). This study cohort included 170 females aged 40 to 45 years who were categorized according to the presentation of MetS components (e.g., central obesity, insulin resistance, atherogenic dyslipidemia, and elevated systolic blood pressure) as controls not presenting a single component (n = 43), those with pre-MetS displaying one to two components (n = 70), and females manifesting MetS, e.g., ≥3 components (n = 53). We analyzed the trends of seventeen oxidative and nine inflammatory status markers across three clinical categories. A multivariate regression of selected oxidative status and inflammatory markers on the components of MetS was performed. Markers of oxidative damage (malondialdehyde and advanced-glycation-end-products-associated fluorescence of plasma) were similar across the groups. Healthy controls displayed lower uricemia and higher bilirubinemia than females with MetS; and lower leukocyte counts, concentrations of C-reactive protein, interleukine-6, and higher levels of carotenoids/lipids and soluble receptors for advanced glycation end-products than those with pre-MetS and MetS. In multivariate regression models, levels of C-reactive protein, uric acid, and interleukine-6 were consistently associated with MetS components, although the impacts of single markers differed. Our data suggest that a proinflammatory imbalance precedes the manifestation of MetS, while an imbalance of oxidative status accompanies overt MetS. Further studies are needed to elucidate whether determining markers beyond traditional ones could help improve the prognosis of subjects at an early stage of MetS. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Metabolic Syndrome)

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17 pages, 343 KiB

Open AccessArticle

Polyunsaturated and Saturated Oxylipin Plasma Levels Allow Monitoring the Non-Alcoholic Fatty Liver Disease Progression to Severe Stages

by Miguel D. Ferrer, Clara Reynés, Margalida Monserrat-Mesquida, Magdalena Quetglas-Llabrés, Cristina Bouzas, Silvia García, David Mateos, Miguel Casares, Cristina Gómez, Lucía Ugarriza, Josep A. Tur, Antoni Sureda and Antoni Pons

Antioxidants 2023, 12(3), 711; https://doi.org/10.3390/antiox12030711 - 13 Mar 2023

Cited by 6 | Viewed by 2091

Abstract

Hepatic fat accumulation is the hallmark of non-alcoholic fatty liver disease (NAFLD). Our aim was to determine the plasma levels of oxylipins, free polyunsaturated fatty acids (PUFA) and markers of lipid peroxidation in patients with NAFLD in progressive stages of the pathology. Ninety 40–60-year-old adults diagnosed with metabolic syndrome were distributed in without, mild, moderate or severe NAFLD stages. The free PUFA and oxylipin plasma levels were determined by the UHPLC–MS/MS system. The plasma levels of oxylipins produced by cyclooxygenases, lipoxygenases and cytochrome P450, such as prostaglandin 2α (PGF2α), lipoxinB4 and maresin-1, were higher in severe NAFLD patients, pointing to the coexistence of both inflammation and resolution processes. The plasma levels of the saturated oxylipins 16-hydroxyl-palmitate and 3-hydroxyl-myristate were also higher in the severe NAFLD patients, suggesting a dysregulation of oxidation of fatty acids. The plasma 12-hydroxyl-estearate (12HEST) levels in severe NAFLD were higher than in the other stages, indicating that the hydroxylation of saturated fatty acid produced by reactive oxygen species is more present in this severe stage of NAFLD. The plasma levels of 12HEST and PGF2α are potential candidate biomarkers for diagnosing NAFLD vs. non-NAFLD. In conclusion, the NAFLD progression can be monitored by measuring the plasma levels of free PUFA and oxylipins characterizing the different NAFLD stages or the absence of this disease in metabolic syndrome patients. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Metabolic Syndrome)

18 pages, 7636 KiB

Open AccessArticle

CHIP Haploinsufficiency Exacerbates Hepatic Steatosis via Enhanced TXNIP Expression and Endoplasmic Reticulum Stress Responses

by Jung-Hwa Han, Dae-Hwan Nam, Seon-Hui Kim, Ae-Rang Hwang, So-Young Park, Jae Hyang Lim and Chang-Hoon Woo

Antioxidants 2023, 12(2), 458; https://doi.org/10.3390/antiox12020458 - 11 Feb 2023

Cited by 1 | Viewed by 2526

Abstract

TXNIP is a critical regulator of glucose homeostasis, fatty acid synthesis, and cholesterol accumulation in the liver, and it has been reported that metabolic diseases, such as obesity, atherosclerosis, hyperlipidemia, type 2 diabetes, and nonalcoholic fatty liver disease (NAFLD), are associated with endoplasmic reticulum (ER) stress. Because CHIP, an E3 ligase, was known to be involved in regulating tissue injury and inflammation in liver, its role in regulating ER stress-induced NAFLD was investigated in two experimental NAFLD models, a tunicamycin (TM)-induced and other diet-induced NAFLD mice models. In the TM-induced NAFLD model, intraperitoneal injection of TM induced liver steatosis in both CHIP^+/+ and CHIP^+/− mice, but it was severely exacerbated in CHIP^+/− mice compared to CHIP^+/+ mice. Key regulators of ER stress and de novo lipogenesis were also enhanced in the livers of TM-inoculated CHIP^+/− mice. Furthermore, in the diet-induced NAFLD models, CHIP^+/− mice developed severely impaired glucose tolerance, insulin resistance and hepatic steatosis compared to CHIP^+/+ mice. Interestingly, CHIP promoted ubiquitin-dependent degradation of TXNIP in vitro, and inhibition of TXNIP was further found to alleviate the inflammation and ER stress responses increased by CHIP inhibition. In addition, the expression of TXNIP was increased in mice deficient in CHIP in the TM- and diet-induced models. These findings suggest that CHIP modulates ER stress and inflammatory responses by inhibiting TXNIP, and that CHIP protects against TM- or HF–HS diet-induced NAFLD and serves as a potential therapeutic means for treating liver diseases. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Metabolic Syndrome)

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20 pages, 3841 KiB

Open AccessArticle

Dietary Mg Supplementation Decreases Oxidative Stress, Inflammation, and Vascular Dysfunction in an Experimental Model of Metabolic Syndrome with Renal Failure

by Rodrigo López-Baltanás, María E. Rodríguez-Ortiz, Juan M. Díaz-Tocados, Julio M. Martinez-Moreno, Cristina Membrives, Cristian Rodelo-Haad, M. Victoria Pendón Ruiz de Mier, Mariano Rodríguez, Antonio Canalejo, Yolanda Almadén and Juan R. Muñoz-Castañeda

Antioxidants 2023, 12(2), 283; https://doi.org/10.3390/antiox12020283 - 27 Jan 2023

Cited by 4 | Viewed by 2646

Abstract

Background: Metabolic syndrome (MetS) and chronic kidney disease (CKD) are commonly associated with cardiovascular disease (CVD) and in these patients Mg concentration is usually decreased. This study evaluated whether a dietary Mg supplementation might attenuate vascular dysfunction through the modulation of oxidative stress and inflammation in concurrent MetS and CKD. Methods: A rat model of MetS (Zucker strain) with CKD (5/6 nephrectomy, Nx) was used. Nephrectomized animals were fed a normal 0.1%Mg (MetS+Nx+Mg0.1%) or a supplemented 0.6%Mg (MetS+Nx+Mg0.6%) diet; Sham-operated rats with MetS receiving 0.1%Mg were used as controls. Results: As compared to controls, the MetS+Nx-Mg0.1% group showed a significant increase in oxidative stress and inflammation biomarkers (lipid peroxidation and aortic interleukin-1b and -6 expression) and Endothelin-1 levels, a decrease in nitric oxide and a worsening in uremia and MetS associated pathology as hypertension, and abnormal glucose and lipid profile. Moreover, proteomic evaluation revealed changes mainly related to lipid metabolism and CVD markers. By contrast, in the MetS+Nx+Mg0.6% group, these parameters remained largely similar to controls. Conclusion: In concurrent MetS and CKD, dietary Mg supplementation reduced inflammation and oxidative stress and improved vascular function. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Metabolic Syndrome)

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18 pages, 1040 KiB

Open AccessArticle

The Antioxidant Potential of the Mediterranean Diet as a Predictor of Weight Loss after a Very Low-Calorie Ketogenic Diet (VLCKD) in Women with Overweight and Obesity

by Ludovica Verde, Maria Dalamaga, Xavier Capó, Giuseppe Annunziata, Maria Hassapidou, Annamaria Docimo, Silvia Savastano, Annamaria Colao, Giovanna Muscogiuri and Luigi Barrea

Antioxidants 2023, 12(1), 18; https://doi.org/10.3390/antiox12010018 - 22 Dec 2022

Cited by 20 | Viewed by 4314

Abstract

Obesity involves a chronic state of low-grade inflammation, which is linked to the development of several comorbidities. Recently, the very low-calorie ketogenic diet (VLCKD) has gained great interest in the treatment of obesity, almost ousting the ancient and healthy Mediterranean diet (MD). However, because these dietary regimens exploit different pathophysiological mechanisms, we hypothesize that adherence to the MD may play a role in determining the efficacy of the VLCKD. We enrolled 318 women (age 38.84 ± 14.37 years; BMI 35.75 ± 5.18 kg/m²) and assessed their anthropometric parameters, body compositions, and adherence to the MD (with the PREvención con DIetaMEDiterránea (PREDIMED) questionnaire) at baseline. The anthropometric parameters and body composition were repeated at the end of the VLCKD. At the end of the VLCKD, the women with high adherence to the MD achieved the best results in terms of weight loss and improved body composition. Specifically, the women who were above the median of fat mass (FM)% reduction had the best MD pattern, characterized by a higher consumption of extra virgin olive oil (EVOO), fruits, vegetables, and red wine, as well as a higher adherence to the MD than the women who were below the same median. In a multiple regression analysis, the PREDIMED score was the main predictor of the FM% reduction score and came in first, followed by fruit, EVOO, and glasses of wine, in predicting the percentage reduction in FM. A PREDIMED score value of > 5 could serve as a threshold to identify patients who are more likely to lose FM at the end of the VLCKD. In conclusion, high adherence to the MD resulted in higher VLCKD efficacy. This could be due to the antioxidant and anti-inflammatory properties of the MD, which are capable of establishing a metabolic set-up that is favorable to the onset of more effective ketosis. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Metabolic Syndrome)

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21 pages, 1532 KiB

Open AccessReview

Redox Balance in Type 2 Diabetes: Therapeutic Potential and the Challenge of Antioxidant-Based Therapy

by Lital Argaev-Frenkel and Tovit Rosenzweig

Antioxidants 2023, 12(5), 994; https://doi.org/10.3390/antiox12050994 - 25 Apr 2023

Cited by 11 | Viewed by 2370

Abstract

Oxidative stress is an important factor in the development of type 2 diabetes (T2D) and associated complications. Unfortunately, most clinical studies have failed to provide sufficient evidence regarding the benefits of antioxidants (AOXs) in treating this disease. Based on the known complexity of reactive oxygen species (ROS) functions in both the physiology and pathophysiology of glucose homeostasis, it is suggested that inappropriate dosing leads to the failure of AOXs in T2D treatment. To support this hypothesis, the role of oxidative stress in the pathophysiology of T2D is described, together with a summary of the evidence for the failure of AOXs in the management of diabetes. A comparison of preclinical and clinical studies indicates that suboptimal dosing of AOXs might explain the lack of benefits of AOXs. Conversely, the possibility that glycemic control might be adversely affected by excess AOXs is also considered, based on the role of ROS in insulin signaling. We suggest that AOX therapy should be given in a personalized manner according to the need, which is the presence and severity of oxidative stress. With the development of gold-standard biomarkers for oxidative stress, optimization of AOX therapy may be achieved to maximize the therapeutic potential of these agents. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Metabolic Syndrome)

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19 pages, 1618 KiB

Open AccessReview

Impaired Melatonin Secretion, Oxidative Stress and Metabolic Syndrome in Night Shift Work

by Sorina Hohor, Cristina Mandanach, Andreea Maftei, Corina Aurelia Zugravu and Marina Ruxandra Oțelea

Antioxidants 2023, 12(4), 959; https://doi.org/10.3390/antiox12040959 - 19 Apr 2023

Cited by 7 | Viewed by 3004

Abstract

Metabolic syndrome has been associated in many studies with working in shifts. Even if the mechanistic details are not fully understood, forced sleep deprivation and exposure to light, as happens during night shifts, or irregular schedules with late or very early onset of the working program, lead to a sleep–wake rhythm misalignment, metabolic dysregulation and oxidative stress. The cyclic melatonin secretion is regulated by the hypothalamic suprachiasmatic nuclei and light exposure. At a central level, melatonin promotes sleep and inhibits wake-signals. Beside this role, melatonin acts as an antioxidant and influences the functionality of the cardiovascular system and of different metabolic processes. This review presents data about the influence of night shifts on melatonin secretion and oxidative stress. Assembling data from epidemiological, experimental and clinical studies contributes to a better understanding of the pathological links between chronodisruption and the metabolic syndrome related to working in shifts. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Metabolic Syndrome)

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18 pages, 1731 KiB

Open AccessReview

Potential Role of Oxidative Stress in the Production of Volatile Organic Compounds in Obesity

by Adebowale Samuel Oyerinde, Vaithinathan Selvaraju, Jeganathan Ramesh Babu and Thangiah Geetha

Antioxidants 2023, 12(1), 129; https://doi.org/10.3390/antiox12010129 - 5 Jan 2023

Cited by 22 | Viewed by 4127

Abstract

Obesity is associated with numerous health issues such as sleep disorders, asthma, hepatic dysfunction, cancer, renal dysfunction, diabetes, cardiovascular complications, and infertility. Previous research has shown that the distribution of excess body fat, rather than excess body weight, determines obesity-related risk factors. It is widely accepted that abdominal fat is a serious risk factor for illnesses associated with obesity and the accumulation of visceral fat promotes the release of pro-oxidants, pro-inflammatory, and reactive oxygen species (ROS). The metabolic process in the human body produces several volatile organic compounds (VOCs) via urine, saliva, breath, blood, skin secretions, milk, and feces. Several studies have shown that VOCs are released by the interaction of ROS with underlying cellular components leading to increased protein oxidation, lipid peroxidation, or DNA damage. These VOCs released via oxidative stress in obese individuals may serves as a biomarker for obesity-related metabolic alterations and disease. In this review, we focus on the relationship between oxidative stress and VOCs in obesity. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Metabolic Syndrome)

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23 pages, 1383 KiB

Open AccessReview

Metabolic Syndrome Programming and Reprogramming: Mechanistic Aspects of Oxidative Stress

by You-Lin Tain and Chien-Ning Hsu

Antioxidants 2022, 11(11), 2108; https://doi.org/10.3390/antiox11112108 - 26 Oct 2022

Cited by 10 | Viewed by 2456

Abstract

Metabolic syndrome (MetS) is a worldwide public health issue characterized by a set of risk factors for cardiovascular disease. MetS can originate in early life by developmental programming. Increasing evidence suggests that oxidative stress, which is characterized as an imbalance between reactive oxygen species (ROS), nitric oxide (NO), and antioxidant systems, plays a decisive role in MetS programming. Results from human and animal studies indicate that maternal-derived insults induce MetS later in life, accompanied by oxidative stress programming of various organ systems. On the contrary, perinatal use of antioxidants can offset oxidative stress and thereby prevent MetS traits in adult offspring. This review provides an overview of current knowledge about the core mechanisms behind MetS programming, with particular focus on the occurrence of oxidative-stress-related pathogenesis as well as the use of potential oxidative-stress-targeted interventions as a reprogramming strategy to avert MetS of developmental origins. Future clinical studies should provide important proof of concept for the effectiveness of these reprogramming interventions to prevent a MetS epidemic. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Metabolic Syndrome)

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