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Cells
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Recent Advances of Oxidative Stress and Inflammation in Diabetes
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Recent Advances of Oxidative Stress and Inflammation in Diabetes

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: closed (1 April 2023) | Viewed by 17549

Special Issue Editors

Prof. Dr. Itamar Raz

E-Mail Website
Guest Editor
Diabetes Unit, Department of Endocrinology and Metabolism, Hadassah Medical Center, Hebrew University of Jerusalem, The Faculty of Medicine, Jerusalem 91120, Israel
Interests: insulin resistance; diabetes; lipid metabolism; glucose metabolism; disease prevention; obesity metabolic endocrinology; high fructose corn syrup; cardiovascular disease; obesity; telemedicine; telehealth; eHealth; mHealth; digital health; review; connected diabetes care; diabetes mellitus; glucose monitoring
Special Issues, Collections and Topics in MDPI journals
Dr. Roni Weinberg Sibony

E-Mail
Guest Editor Assistant
Goldman Medical School, Faculty of Health Sciences, Ben Gurion University, Beer Sheva 8410501, Israel
Interests: diabetes; obesity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The pathological progression of diabetes mellitus is intimately connected to the formation and activation of oxidative stress (OS).

OS is a consequence of the redox system disturbance characterized by a notably increased production of reactive oxygen species (ROS)1.

ROS plays a central role in the interactions involving inflammation and metabolic control. Hyperglycemia, through various mechanisms, leads to increased ROS production and chronic inflammation. The excessive production of ROS can feedback and contribute to the pathogenesis of insulin resistance and impaired insulin secretion, a vicious circle that continues to recur.2

Endogenous antioxidant defense systems help to reduce deleterious ROS. Antioxidant enzymes can accelerate the breakdown of ROS, while the non-enzyme antioxidants can capture and eliminate free radicals.3 Studies show that external antioxidants, such as vitamin C, vitamin E, carotenoids, and various derivatives of phenyl-propenoids, have the potential to enhance antioxidant defense systems. Additionally, the consumption of polyphenol-rich food has been associated with several multitarget antioxidative activities. Particularly, studies have shown gallic acid (GA), the common chemical entity of polyphenols, to be an antioxidant and regulator of immunity to infections.2

Various studies show different endogenous substances that may reduce the OS, for example MitoQTPP and TEMPOL, two mitochondria antioxidants, epigallocatechin gallate, green tea compounds and curcumin.4,5

The purpose of this Special Issue is to highlight the research advances regarding the interactions between oxidative stress and inflammation in diabetes. Our goal is to provide research papers and reviews related to endogenous and external antioxidant defense systems and to present modern therapeutic strategies in the treatment of DM that aim to develop new methods of personalized antioxidant therapy.3

  1. Luc K, Schramm-Luc A, Guzik TJ, Mikolajczyk TP. Oxidative stress and inflammatory markers in prediabetes and diabetes. J Physiol Pharmacol. 2019 Dec;70(6). doi: 10.26402/jpp.2019.6.01. Epub 2020 Feb 19. PMID: 32084643.
  2. Yu Xu, Guoyi Tank, Cheng zhang. Gallic Acid and diabetis mellitus: its association with oxidative stress. 2021 Nov, Moleculum.
  3. Darenskaya MA, Kolesnikova LI, Kolesnikov SI. Oxidative Stress: Pathogenetic Role in Diabetes Mellitus and Its Complications and Therapeutic Approaches to Correction. Bull Exp Biol Med. 2021 May;171(2):179-189. doi: 10.1007/s10517-021-05191-7. Epub 2021 Jun 26. PMID: 34173093; PMCID: PMC8233182.
  4. Bulboaca AE, Boarescu PM, Porfre AS, Dogaru G, Barbalata C, Valeanu M, Munteanu C, Râjnoveanu RM, Nicula CA, Stanescu IC. The efect of nano-epigallocatechin-gallate on oxidative stress and matrix metalloproteinases in experimental diabetes mellitus. Antioxidants (Basel). 2020;9(2):172. doi: 10.3390/antiox9020172
  5. Pivari F, Mingione A, Brasacchio C, Soldati L. Curcumin and type 2 diabetes mellitus: prevention and treatment. Nutrients. 2019;11(8):1837. doi: 10.3390/nu11081837

Prof. Dr. Itamar Raz
Guest Editor
Roni Weinberg Sibony
Guest Editor Assistant

Manuscript Submission Information

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Keywords

  • diabetes mellitus
  • oxidative stress
  • inflammation
  • hyperglycemia
  • reactive oxygen species
  • antioxidants
  • β cells
  • gallic acid

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Related Special Issue

Published Papers (6 papers)

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Research

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23 pages, 4882 KiB  
Article
Cardiovascular Protective Effects of NP-6A4, a Drug with the FDA Designation for Pediatric Cardiomyopathy, in Female Rats with Obesity and Pre-Diabetes
by Anthony M. Belenchia, Asma Boukhalfa, Vincent G. DeMarco, Alexander Mehm, Abuzar Mahmood, Pei Liu, Yinian Tang, Madhavi P. Gavini, Brian Mooney, Howard H. Chen and Lakshmi Pulakat
Cells 2023, 12(10), 1373; https://doi.org/10.3390/cells12101373 - 12 May 2023
Cited by 4 | Viewed by 2290
Abstract
Background: Obese and pre-diabetic women have a higher risk for cardiovascular death than age-matched men with the same symptoms, and there are no effective treatments. We reported that obese and pre-diabetic female Zucker Diabetic Fatty (ZDF-F) rats recapitulate metabolic and cardiac pathology of [...] Read more.
Background: Obese and pre-diabetic women have a higher risk for cardiovascular death than age-matched men with the same symptoms, and there are no effective treatments. We reported that obese and pre-diabetic female Zucker Diabetic Fatty (ZDF-F) rats recapitulate metabolic and cardiac pathology of young obese and pre-diabetic women and exhibit suppression of cardio-reparative AT2R. Here, we investigated whether NP-6A4, a new AT2R agonist with the FDA designation for pediatric cardiomyopathy, mitigate heart disease in ZDF-F rats by restoring AT2R expression. Methods: ZDF-F rats on a high-fat diet (to induce hyperglycemia) were treated with saline, NP-6A4 (10 mg/kg/day), or NP-6A4 + PD123319 (AT2R-specific antagonist, 5 mg/kg/day) for 4 weeks (n = 21). Cardiac functions, structure, and signaling were assessed by echocardiography, histology, immunohistochemistry, immunoblotting, and cardiac proteome analysis. Results: NP-6A4 treatment attenuated cardiac dysfunction, microvascular damage (−625%) and cardiomyocyte hypertrophy (−263%), and increased capillary density (200%) and AT2R expression (240%) (p < 0.05). NP-6A4 activated a new 8-protein autophagy network and increased autophagy marker LC3-II but suppressed autophagy receptor p62 and autophagy inhibitor Rubicon. Co-treatment with AT2R antagonist PD123319 suppressed NP-6A4’s protective effects, confirming that NP-6A4 acts through AT2R. NP-6A4-AT2R-induced cardioprotection was independent of changes in body weight, hyperglycemia, hyperinsulinemia, or blood pressure. Conclusions: Cardiac autophagy impairment underlies heart disease induced by obesity and pre-diabetes, and there are no drugs to re-activate autophagy. We propose that NP-6A4 can be an effective drug to reactivate cardiac autophagy and treat obesity- and pre-diabetes-induced heart disease, particularly for young and obese women. Full article
(This article belongs to the Special Issue Recent Advances of Oxidative Stress and Inflammation in Diabetes)
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10 pages, 811 KiB  
Communication
Oxidative Stress in Postmenopausal Women with or without Obesity
by Giulia Leanza, Caterina Conte, Francesca Cannata, Camilla Isgrò, Alessandra Piccoli, Rocky Strollo, Carlo Cosimo Quattrocchi, Rocco Papalia, Vincenzo Denaro, Mauro Maccarrone, Nicola Napoli and Anna Maria Sardanelli
Cells 2023, 12(8), 1137; https://doi.org/10.3390/cells12081137 - 12 Apr 2023
Cited by 9 | Viewed by 2432
Abstract
Oxidative stress, a key mediator of cardiovascular disease, metabolic alterations, and cancer, is independently associated with menopause and obesity. Yet, among postmenopausal women, the correlation between obesity and oxidative stress is poorly examined. Thus, in this study, we compared oxidative stress states in [...] Read more.
Oxidative stress, a key mediator of cardiovascular disease, metabolic alterations, and cancer, is independently associated with menopause and obesity. Yet, among postmenopausal women, the correlation between obesity and oxidative stress is poorly examined. Thus, in this study, we compared oxidative stress states in postmenopausal women with or without obesity. Body composition was assessed via DXA, while lipid peroxidation and total hydroperoxides were measured in patient’s serum samples via thiobarbituric-acid-reactive substances (TBARS) and derivate-reactive oxygen metabolites (d-ROMs) assays, respectively. Accordingly, 31 postmenopausal women were enrolled: 12 with obesity and 19 of normal weight (mean (SD) age 71.0 (5.7) years). Doubled levels of serum markers of oxidative stress were observed in women with obesity in women with obesity compared to those of normal weight (H2O2: 32.35 (7.3) vs. 18.80 (3.4) mg H2O2/dL; malondialdehyde (MDA): 429.6 (138.1) vs. 155.9 (82.4) mM in women with or without obesity, respectively; p < 0.0001 for both). Correlation analysis showed that both markers of oxidative stress increased with an increasing body mass index (BMI), visceral fat mass, and trunk fat percentage, but not with fasting glucose levels. In conclusion, obesity and visceral fat are associated with a greater increase in oxidative stress in postmenopausal women, possibly increasing cardiometabolic and cancer risks. Full article
(This article belongs to the Special Issue Recent Advances of Oxidative Stress and Inflammation in Diabetes)
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11 pages, 532 KiB  
Article
Redox Genetic Risk Score and the Incidence of End-Stage Kidney Disease in People with Type 1 Diabetes
by Kamel Mohammedi, Michel Marre, Samy Hadjadj, Louis Potier and Gilberto Velho
Cells 2022, 11(24), 4131; https://doi.org/10.3390/cells11244131 - 19 Dec 2022
Viewed by 1521
Abstract
End-stage kidney disease (ESKD) is a multifactorial condition influenced by genetic background, but the extent to which a genetic risk score (GRS) improves ESKD prediction is unknown. We built a redox GRS on the base of previous association studies (six polymorphisms from six [...] Read more.
End-stage kidney disease (ESKD) is a multifactorial condition influenced by genetic background, but the extent to which a genetic risk score (GRS) improves ESKD prediction is unknown. We built a redox GRS on the base of previous association studies (six polymorphisms from six redox genes) and tested its relationship with ESKD in three cohorts of people with type 1 diabetes. Among 1012 participants, ESKD (hemodialysis requirement, kidney transplantation, eGFR < 15 mL/min/1.73 m2) occurred in 105 (10.4%) during a 14-year follow-up. High redox GRS was associated with increased ESKD risk (adjusted HR for the upper versus the lowest GRS tertile: 2.60 (95% CI, 1.51–4.48), p = 0.001). Each additional risk-allele was associated with a 20% increased risk of ESKD (95% CI, 8–33, p < 0.0001). High GRS yielded a relevant population attributable fraction (30%), but only a marginal enhancement in c-statistics index (0.928 [0.903–0.954]) over clinical factors 0.921 (0.892–0.950), p = 0.04). This is the first report of an independent association between redox GRS and increased risk of ESKD in type 1 diabetes. Our results do not support the use of this GRS in clinical practice but provide new insights into the involvement of oxidative stress genetic factors in ESKD risk in type 1 diabetes. Full article
(This article belongs to the Special Issue Recent Advances of Oxidative Stress and Inflammation in Diabetes)
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19 pages, 4271 KiB  
Article
Silencing the Adipocytokine NOV: A Novel Approach to Reversing Oxidative Stress-Induced Cardiometabolic Dysfunction
by Maayan Waldman, Shailendra P. Singh, Hsin-Hsueh Shen, Ragin Alex, Rita Rezzani, Gaia Favero, Edith Hochhauser, Ran Kornowski, Michael Arad and Stephen J. Peterson
Cells 2022, 11(19), 3060; https://doi.org/10.3390/cells11193060 - 29 Sep 2022
Cited by 6 | Viewed by 2629
Abstract
Objective: NOV/CCN3 is an adipocytokine recently linked to obesity, insulin resistance, and cardiometabolic dysfunction. NOV is manufactured and secreted from adipose tissue, with blood levels highly correlated with BMI. NOV levels are increased in obesity and a myriad of inflammatory diseases. Elevated NOV [...] Read more.
Objective: NOV/CCN3 is an adipocytokine recently linked to obesity, insulin resistance, and cardiometabolic dysfunction. NOV is manufactured and secreted from adipose tissue, with blood levels highly correlated with BMI. NOV levels are increased in obesity and a myriad of inflammatory diseases. Elevated NOV levels cause oxidative stress by increasing free radicals, decreasing antioxidants, and decreasing heme oxygenase (HO-1) levels, resulting in decreased vascular function. Silencing NOV in NOV knockout mice improved insulin sensitivity. We wanted to study how suppressing NOV expression in an obese animal model affected pathways and processes related to obesity, inflammation, and cardiometabolic function. This is the first study to investigate the interaction of adipose tissue-specific NOV/CCN3 and cardiometabolic function. Methods: We constructed a lentivirus containing the adiponectin-promoter-driven shNOV to examine the effect of NOV inhibition (shNOV) in adipose tissue on the heart of mice fed a high-fat diet. Mice were randomly divided into three groups (five per group): (1) lean (normal diet), (2) high-fat diet (HFD)+ sham virus, and (3) HFD + shNOV lentivirus. Blood pressure, tissue inflammation, and oxygen consumption were measured. Metabolic and mitochondrial markers were studied in fat and heart tissues. Results: Mice fed an HFD developed adipocyte hypertrophy, fibrosis, inflammation, and decreased mitochondrial respiration. Inhibiting NOV expression in the adipose tissue of obese mice by shNOV increased mitochondrial markers for biogenesis (PGC-1α, the nuclear co-activator of HO-1) and functional integrity (FIS1) and insulin signaling (AKT). The upregulation of metabolic and mitochondrial markers was also evident in the hearts of the shNOV mice with the activation of mitophagy. Using RNA arrays, we identified a subgroup of genes that highly correlated with increased adipocyte mitochondrial autophagy in shNOV-treated mice. A heat map analysis in obese mice confirmed that the suppression of NOV overrides the genetic susceptibility of adiposity and the associated detrimental metabolic changes and correlates with the restoration of anti-inflammatory, thermogenic, and mitochondrial genes. Conclusion: Our novel findings demonstrate that inhibiting NOV expression improves adipose tissue function in a positive way in cardiometabolic function by inducing mitophagy and improving mitochondrial function by the upregulation of PGC-1α, the insulin sensitivity signaling protein. Inhibiting NOV expression increases PGC-1, a key component of cardiac bioenergetics, as well as key signaling components of metabolic change, resulting in improved glucose tolerance, improved mitochondrial function, and decreased inflammation. These metabolic changes resulted in increased oxygen consumption, decreased adipocyte size, and improved cardiac metabolism and vascular function at the structural level. The crosstalk of the adipose tissue-specific deletion of NOV/CCN3 improved cardiovascular function, representing a novel therapeutic strategy for obesity-related cardiometabolic dysfunction. Full article
(This article belongs to the Special Issue Recent Advances of Oxidative Stress and Inflammation in Diabetes)
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Review

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28 pages, 4645 KiB  
Review
Early Detection Is the Best Prevention—Characterization of Oxidative Stress in Diabetes Mellitus and Its Consequences on the Cardiovascular System
by Sanela Rajlic, Hendrik Treede, Thomas Münzel, Andreas Daiber and Georg Daniel Duerr
Cells 2023, 12(4), 583; https://doi.org/10.3390/cells12040583 - 11 Feb 2023
Cited by 22 | Viewed by 3420
Abstract
Previous studies demonstrated an important role of oxidative stress in the pathogenesis of cardiovascular disease (CVD) in diabetic patients due to hyperglycemia. CVD remains the leading cause of premature death in the western world. Therefore, diabetes mellitus-associated oxidative stress and subsequent inflammation should [...] Read more.
Previous studies demonstrated an important role of oxidative stress in the pathogenesis of cardiovascular disease (CVD) in diabetic patients due to hyperglycemia. CVD remains the leading cause of premature death in the western world. Therefore, diabetes mellitus-associated oxidative stress and subsequent inflammation should be recognized at the earliest possible stage to start with the appropriate treatment before the onset of the cardiovascular sequelae such as arterial hypertension or coronary artery disease (CAD). The pathophysiology comprises increased reactive oxygen and nitrogen species (RONS) production by enzymatic and non-enzymatic sources, e.g., mitochondria, an uncoupled nitric oxide synthase, xanthine oxidase, and the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX). Considering that RONS originate from different cellular mechanisms in separate cellular compartments, adequate, sensitive, and compartment-specific methods for their quantification are crucial for early detection. In this review, we provide an overview of these methods with important information for early, appropriate, and effective treatment of these patients and their cardiovascular sequelae. Full article
(This article belongs to the Special Issue Recent Advances of Oxidative Stress and Inflammation in Diabetes)
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Other

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8 pages, 614 KiB  
Commentary
The Vagal Nerve, Inflammation, and Diabetes—A Holy Triangle
by Liat Sorski and Yori Gidron
Cells 2023, 12(12), 1632; https://doi.org/10.3390/cells12121632 - 15 Jun 2023
Cited by 7 | Viewed by 3732
Abstract
Type 2 diabetic mellitus (T2DM) is a common chronic disease and a substantial risk factor of other fatal illnesses. At its core is insulin resistance, where chronic low-level inflammation is among its main causes. Thus, it is crucial to modulate this inflammation. This [...] Read more.
Type 2 diabetic mellitus (T2DM) is a common chronic disease and a substantial risk factor of other fatal illnesses. At its core is insulin resistance, where chronic low-level inflammation is among its main causes. Thus, it is crucial to modulate this inflammation. This review paper provides scientific neuroimmunological evidence on the protective roles of the vagal nerve in T2DM. First, the vagus inhibits inflammation in a reflexive manner via neuroendocrine and neuroimmunological routes. This may also occur at the level of brain networks. Second, studies have shown that vagal activity, as indexed by heart-rate variability (HRV), is inversely related to diabetes and that low HRV is a predictor of T2DM. Finally, some emerging evidence shows that vagal nerve activation may reduce biomarkers and processes related to diabetes. Future randomized controlled trials are needed to test the effects of vagal nerve activation on T2DM and its underlying anti-inflammatory mechanisms. Full article
(This article belongs to the Special Issue Recent Advances of Oxidative Stress and Inflammation in Diabetes)
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