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Antioxidants
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Oxidative Stress in Diabetes and Complications
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Oxidative Stress in Diabetes and Complications

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 (20 April 2023) | Viewed by 14026

Special Issue Editor

Dr. Sunmin Park

E-Mail Website
Guest Editor
Department of Food and Nutrition, Obesity/Diabetes Research Center, Hoseo University, Asan 31499, Republic of Korea
Interests: Alzheimer’s disease; insulin resistance; nutritional epidemiology; nutrigenomics; gut microbiome; type 2 diabetes; bioinformatics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Diabetes mellitus is the seventh leading cause of death worldwide and is characterized by high blood glucose concentrations caused by either impaired insulin secretion or sensitivity. Elevated blood glucose is present in all types of diabetes, and elevated lipids is a feature of type 2 diabetes, which accounts for 75% of all diabetes. Many of the most serious complications of diabetes are caused by oxidative damage that is induced by hyperglycemia and hyperlipidemia, which are definitive characteristics of diabetes.

Reactive oxygen species (ROS) exacerbate insulin resistance and impair insulin secretion capacity by killing pancreatic β-cells. Furthermore, ROS can lead to the production of advanced glycation end products (AGES), dysregulation of the polyol pathway, and increased production of lipids and protein-derived ROS. These products have been especially associated with the microvascular (retinopathy, nephropathy, and neuropathy) complications and macrovascular (coronary artery disease, peripheral artery disease, and cerebral vascular disease) complications of diabetes.

This Special Issue of Antioxidants seeks to further explore the causes, consequences, and challenges of treating oxidative processes associated with both the etiologies and pathologies of type 1, type 2, and gestational diabetes mellitus to prevent both the disease progression and the exacerbation of diabetic symptoms and diabetic complications. Interventions that may prevent or reverse the damage caused by ROS generated by diabetes are of special interest. However, both original research and critical reviews providing novel insights into the causes and treatments of pathologies related to diabetes-induced oxidative stress are welcome.

Prof. Dr. Sunmin Park
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • hyperglycemia
  • oxidative stress
  • antioxidants
  • diabetic complications
  • gut microbiome

Published Papers (6 papers)

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Research

20 pages, 2668 KiB  
Article
17β-Estradiol Suppresses Gastric Inflammatory and Apoptotic Stress Responses and Restores nNOS-Mediated Gastric Emptying in Streptozotocin (STZ)-Induced Diabetic Female Mice
by Jeremy Sprouse, Chethan Sampath and Pandu Gangula
Antioxidants 2023, 12(3), 758; https://doi.org/10.3390/antiox12030758 - 20 Mar 2023
Cited by 3 | Viewed by 1734
Abstract
Gastroparesis (Gp) is a severe complication of diabetes mellitus (DM) observed predominantly in women. It is characterized by abnormal gastric emptying (GE) without mechanical obstruction in the stomach. Nitric oxide (NO) is an inhibitory neurotransmitter produced by neuronal nitric oxide synthase (nNOS). It [...] Read more.
Gastroparesis (Gp) is a severe complication of diabetes mellitus (DM) observed predominantly in women. It is characterized by abnormal gastric emptying (GE) without mechanical obstruction in the stomach. Nitric oxide (NO) is an inhibitory neurotransmitter produced by neuronal nitric oxide synthase (nNOS). It plays a critical role in gastrointestinal (GI) motility and stomach emptying. Here, we wanted to demonstrate the protective effects of supplemental 17β-estradiol (E2) on NO-mediated gastric function. We showed E2 supplementation to alleviate oxidative and inflammatory stress in streptozotocin (STZ)-induced diabetic female mice. Our findings suggest that daily administration of E2 at therapeutic doses is beneficial for metabolic homeostasis. This restoration occurs via regulating and modulating the expression/function of glycogen synthase kinase-3β (GSK-3β), nuclear factor-erythroid 2 p45-related factor 2 (Nrf2), Phase II enzymes, MAPK- and nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB)-mediated inflammatory cytokines (IL-1β, IL-6, TNFα, IGF-1), and gastric apoptotic regulators. We also showed E2 supplementation to elevate GCH-1 protein levels in female diabetic mice. Since GCH-1 facilitates the production of tetrahydrobiopterin (BH4, cofactor for nNOS), an increase in GCH-1 protein levels in diabetic mice may improve their GE and nitrergic function. Our findings provide new insights into the impact of estrogen on gastric oxidative stress and intracellular inflammatory cascades in the context of Gp. Full article
(This article belongs to the Special Issue Oxidative Stress in Diabetes and Complications)
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11 pages, 2891 KiB  
Article
Cytoprotective Effect of Pteryxin on Insulinoma MIN6 Cells Due to Antioxidant Enzymes Expression via Nrf2/ARE Activation
by Junsei Taira, Ryuji Tsuda, Chika Miyagi-Shiohira, Hirofumi Noguchi and Takayuki Ogi
Antioxidants 2023, 12(3), 693; https://doi.org/10.3390/antiox12030693 - 10 Mar 2023
Cited by 1 | Viewed by 1363
Abstract
The low-level antioxidant activity of pancreatic islets causes type 1 diabetes due to oxidative stress, which is also the cause of failure in the pancreatic islets’ isolation and cell transplantation. In our previous study, pteryxin was found to be a natural product as [...] Read more.
The low-level antioxidant activity of pancreatic islets causes type 1 diabetes due to oxidative stress, which is also the cause of failure in the pancreatic islets’ isolation and cell transplantation. In our previous study, pteryxin was found to be a natural product as a nuclear factor-erythroid-2-related factor (Nrf2) activator. This study focused on elucidation that the potentiality of pteryxin can activate the antioxidant enzymes, even under oxidative stress, by hydrogen peroxide (H2O2). Pteryxin treated with mouse insulinoma MIN6 cells was enhanced the antioxidant gene expressions in the ARE (antioxidant response element) region for HO-1 (Heme Oxygenase-1), GCLC (Glutamate-cysteine ligase catalytic subunit), SOD1 (Super Oxide dismutase1), and Trxr1 (Thioredoxin reductase1), and those enzymes were also expressed during the nuclei transference of cytoplasmic Nrf2. In fact, the cells exposed to H2O2 concentrations of a half-cell lethal in the presence of pteryxin were then induced main antioxidant enzymes, HO-1, GCLC, and Trxr1 in the ARE region. The increased glutathione (GSH) levels associated with the GCLC expression also suggested to be cytoprotective against oxidative stress by activating the redox-metabolizing enzymes involving their increased antioxidant activity in the cells. In addition, Akt is a modulator for Nrf2, which may be responsible for the Nrf2 activation. These results allowed us to consider whether pteryxin or its synthesized congeners, an Nrf2 activator, is a potential preservative agent against islet isolation during cell transplantation. Full article
(This article belongs to the Special Issue Oxidative Stress in Diabetes and Complications)
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16 pages, 4876 KiB  
Article
Gold Nanoparticles Supported on Ceria Nanoparticles Modulate Leukocyte–Endothelium Cell Interactions and Inflammation in Type 2 Diabetes
by Pedro Díaz-Pozo, Francisco Canet, Abdessamad Grirrane, Sandra Lopez-Domenech, José Raul Herance, Nadezda Apostolova, Clara Luna-Marco, Susana Rovira-Llopis, Miguel Marti, Carlos Morillas, Milagros Rocha, Hermenegildo Garcia and Victor M. Victor
Antioxidants 2022, 11(11), 2297; https://doi.org/10.3390/antiox11112297 - 20 Nov 2022
Cited by 3 | Viewed by 2147
Abstract
Gold-ceria nanoparticles (Au/CeO2) are known to have antioxidant properties. However, whether these nanoparticles can provide benefits in type 2 diabetes mellitus (T2D) remains unknown. This work aimed to study the effects of Au/CeO2 nanoparticles at different rates of gold purity [...] Read more.
Gold-ceria nanoparticles (Au/CeO2) are known to have antioxidant properties. However, whether these nanoparticles can provide benefits in type 2 diabetes mellitus (T2D) remains unknown. This work aimed to study the effects of Au/CeO2 nanoparticles at different rates of gold purity (10, 4.4, 1.79 and 0.82) on leukocyte–endothelium interactions and inflammation in T2D patients. Anthropometric and metabolic parameters, leukocyte–endothelium interactions, ROS production and NF-κB expression were assessed in 57 T2D patients and 51 healthy subjects. T2D patients displayed higher Body Mass Index (BMI) and characteristic alterations in carbohydrate and lipid metabolism. ROS production was increased in leukocytes of T2D patients and decreased by Au/CeO2 at 0.82% gold. Interestingly, Au/CeO2 0.82% modulated leukocyte–endothelium interactions (the first step in the atherosclerotic process) by increasing leukocyte rolling velocity and decreasing rolling flux and adhesion in T2D. A static adhesion assay also revealed diminished leukocyte–endothelium interactions by Au/CeO2 0.82% treatment. NF-κB (p65) levels increased in T2D patients and were reduced by Au/CeO2 treatment. Cell proliferation, viability, and apoptosis assays demonstrated no toxicity produced by Au/CeO2 nanoparticles. These results demonstrate that Au/CeO2 nanoparticles at 0.82% exert antioxidant and anti-inflammatory actions in the leukocyte–endothelium interaction of T2D patients, suggesting a protective role against the appearance of atherosclerosis and cardiovascular diseases when this condition exists. Full article
(This article belongs to the Special Issue Oxidative Stress in Diabetes and Complications)
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22 pages, 4070 KiB  
Article
Low-Dose Dioxin Reduced Glucose Uptake in C2C12 Myocytes: The Role of Mitochondrial Oxidative Stress and Insulin-Dependent Calcium Mobilization
by Suyeol Im, Sora Kang, Ji Hwan Kim, Seung Jun Oh and Youngmi Kim Pak
Antioxidants 2022, 11(11), 2109; https://doi.org/10.3390/antiox11112109 - 26 Oct 2022
Cited by 2 | Viewed by 2211
Abstract
Chronic exposure to some environmental polluting chemicals (EPCs) is strongly associated with metabolic syndrome, and insulin resistance is a major biochemical abnormality in the skeletal muscle in patients with metabolic syndrome. However, the causal relationship is inconsistent and little is known about how [...] Read more.
Chronic exposure to some environmental polluting chemicals (EPCs) is strongly associated with metabolic syndrome, and insulin resistance is a major biochemical abnormality in the skeletal muscle in patients with metabolic syndrome. However, the causal relationship is inconsistent and little is known about how EPCs affect the insulin signaling cascade in skeletal muscle. Here, we investigated whether exposure to 100 pM of 2,3,7,8-tetrachlorodibenzodioxin (TCDD) as a low dose of dioxin induces insulin resistance in C2C12 myocytes. The treatment with TCDD inhibited the insulin-stimulated glucose uptake and translocation of glucose transporter 4 (GLUT4). The low-dose TCDD reduced the expression of insulin receptor β (IRβ) and insulin receptor substrate (IRS)-1 without affecting the phosphorylation of Akt. The TCDD impaired mitochondrial activities, leading to reactive oxygen species (ROS) production and the blockage of insulin-induced Ca2+ release. All TCDD-mediated effects related to insulin resistance were still observed in aryl hydrocarbon receptor (AhR)-deficient myocytes and prevented by MitoTEMPO, a mitochondria-targeting ROS scavenger. These results suggest that low-dose TCDD stress may induce muscle insulin resistance AhR-independently and that mitochondrial oxidative stress is a novel therapeutic target for dioxin-induced insulin resistance. Full article
(This article belongs to the Special Issue Oxidative Stress in Diabetes and Complications)
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13 pages, 1735 KiB  
Article
Hydrogen Sulfide Regulates Irisin and Glucose Metabolism in Myotubes and Muscle of HFD-Fed Diabetic Mice
by Rajesh Parsanathan and Sushil K. Jain
Antioxidants 2022, 11(7), 1369; https://doi.org/10.3390/antiox11071369 - 14 Jul 2022
Cited by 9 | Viewed by 2108
Abstract
Irisin, a novel myokine, is secreted by the muscle following proteolytic cleavage of fibronectin type III domain containing 5 (FNDC5) and is considered a novel regulator of glucose homeostasis. Cystathionine γ-lyase (CSE) produces hydrogen sulfide (H2S) and is involved in glucose [...] Read more.
Irisin, a novel myokine, is secreted by the muscle following proteolytic cleavage of fibronectin type III domain containing 5 (FNDC5) and is considered a novel regulator of glucose homeostasis. Cystathionine γ-lyase (CSE) produces hydrogen sulfide (H2S) and is involved in glucose homeostasis. We examined the hypothesis that H2S deficiency leads to decreased FNDC5 and irisin secretion, and thereby alters glucose metabolism. High-fat diet-fed mice exhibited elevated blood glucose and significantly reduced levels of CSE, H2S, and PGC-1α, with decreased FNDC5/irisin levels and increased oxidative stress in the muscle compared with those of normal diet-fed mice (control). High glucose or palmitate decreases CSE/PGC-1α/FNDC5 levels and glucose uptake in myotubes. Inhibitors (propargylglycine and aminooxyacetate) of H2S producing enzymes or CSE siRNA significantly decreased levels of H2S and FNDC5 along with PGC-1α; similar H2S-deficient conditions also resulted in decreased GLUT4 and glucose uptake. The levels of H2S, PGC-1α, and FNDC5 and glucose uptake were significantly upregulated after treatment with l-cysteine or an H2S donor. Myoblast differentiation showed upregulation of PGC-1α and FNDC5, which was consistent with the increased expression of CSE/H2S. These findings suggest that the upregulation of H2S levels can have beneficial effects on glucose homeostasis via activation of the PGC-1α/FNDC5/irisin signaling pathway. Full article
(This article belongs to the Special Issue Oxidative Stress in Diabetes and Complications)
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18 pages, 3236 KiB  
Article
A Causal Relationship between Vitamin C Intake with Hyperglycemia and Metabolic Syndrome Risk: A Two-Sample Mendelian Randomization Study
by Meiling Liu and Sunmin Park
Antioxidants 2022, 11(5), 857; https://doi.org/10.3390/antiox11050857 - 27 Apr 2022
Cited by 12 | Viewed by 3380
Abstract
Excessive oxidative stress can contribute to metabolic syndrome (MetS), and antioxidants can protect against its development. Vitamin C (VC) is a well-known antioxidant, and observational studies have associated a deficiency with an increased MetS risk. This study tested the hypothesis that dietary VC [...] Read more.
Excessive oxidative stress can contribute to metabolic syndrome (MetS), and antioxidants can protect against its development. Vitamin C (VC) is a well-known antioxidant, and observational studies have associated a deficiency with an increased MetS risk. This study tested the hypothesis that dietary VC intake caused an inverse relation of MetS and its components risk using a two-sample Mendelian randomization (MR) method in adults ≥40 years in a city hospital-based (n = 58,701) and Ansan/Ansung plus rural (n = 13,598) cohorts. Independent genetic variants associated with dietary VC intake were explored using a genome-wide association study (GWAS) with significance levels of p < 5 × 10−5 and linkage disequilibrium (r2 threshold of 0.001), after adjusting for the covariates related to MetS, in a city hospital-based cohort (n = 52,676) excluding the participants having vitamin supplementation. MR methods, including inverse-variance weighting (IVW), weighted median, MR-Egger, and weighted model, were used to determine the causal relationship between the dietary VC intake and the risk of MetS and its components in Ansan/Ansung plus rural cohorts (n = 11,733). Heterogeneity and leave-one-out sensitivity analyses were conducted. Energy intake, as well as other nutrient intakes, were significantly lower in the low VC intake group than in the high VC intake group, but the incidence of MetS and its components, including hyperglycemia, hypertriglyceridemia, and hypertension, was observationally higher in inadequate low VC intake in the combined cohorts. In MR analysis, insufficient dietary VC intake increased the risk of MetS, hyperglycemia, hypertriglyceridemia, and hypertension in an IVW (p < 0.05). In contrast, only the serum fasting blood glucose concentration was significantly associated with VC intake in weight median analysis (p < 0.05), but there was no significant association of low dietary VC with MetS and its components in MR-Egger. There was no likelihood of heterogeneity and horizontal pleiotropy in MetS and its components. A single genetic variant did not affect their association in the leave-one-out sensitivity analysis. In conclusion, insufficient dietary VC intake potentially increased the MetS and hyperglycemia risk in Asian adults. Low VC intake can contribute to increasing type 2 diabetes incidence in Asians. Full article
(This article belongs to the Special Issue Oxidative Stress in Diabetes and Complications)
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