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Mitochondrial Dysfunction and Oxidative Stress in Diabetes and Associated Diseases

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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 (31 October 2021) | Viewed by 35731

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Dr. Cristina Carvalho

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Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal
Interests: type 2 diabetes; mitochondrial dysfunction; neurodegenerative diseases; oxidative stress; cell (DYS)metabolism
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Dear Colleagues,

Over the last few decades, an increased incidence of diabetes has been observed worldwide, reaching epidemic proportions, and diabetes is currently considered one of the main threats to human health. Diabetes is a chronic metabolic disorder that stems from the fallout from a complex interplay between genetic predisposition and environmental factors, and its burden continues to rise due to changes in lifestyle, affecting about 6% of world’s adult population. Presently, the World Health Organization recognizes three major forms of diabetes: type 1 diabetes (T1D) type 2 diabetes (T2D), and gestational diabetes. Despite different etiologies, defects in mitochondrial function and oxidative stress are a common denominator among all forms. Over time, high glucose levels in the bloodstream can lead to severe complications, such as vision loss, cardiovascular diseases, kidney disorders, nerve damage, and brain degeneration. Thus, studies addressing whether and how changes in mitochondrial metabolism influence the development of diabetes and its associated complications are of great interest.

We invite you to submit your latest research findings or a review article to this Special Issue, which will bring together current research concerning mitochondrial and oxidative stress roles in boosting the incidence of diabetes and its associated complications. This research can include both in vitro and in vivo studies relating to mitochondrial alterations and oxidative stress in any of the following topics: inflammation, obesity, vascular alterations, gender susceptibility, lifestyle (e.g., physical exercise), maternally inherit defects, and microbiota regulation of microbiota function, among others.

Dr. Cristina Carvalho
Guest Editor

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Keywords

Diabetes inflammation
Mitochondrial dysfunction in diabetes
Oxidative stress in diabetes
Diabetes-associated complications
Vascular alterations
Microbiota regulation of mitochondrial function
Obesity
Physical exercise and diabetes
Maternally inherited mitochondrial defects in diabetes

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Research

Jump to: Review

14 pages, 1449 KiB

Open AccessArticle

Melatonin Enhances the Mitochondrial Functionality of Brown Adipose Tissue in Obese—Diabetic Rats

by Ahmad Agil, Miguel Navarro-Alarcon, Fatma Abo Zakaib Ali, Ashraf Albrakati, Diego Salagre, Cristina Campoy and Ehab Kotb Elmahallawy

Antioxidants 2021, 10(9), 1482; https://doi.org/10.3390/antiox10091482 - 17 Sep 2021

Cited by 23 | Viewed by 4048

Abstract

Developing novel drugs/targets remains a major effort toward controlling obesity-related type 2 diabetes (diabesity). Melatonin controls obesity and improves glucose homeostasis in rodents, mainly via the thermogenic effects of increasing the amount of brown adipose tissue (BAT) and increases in mitochondrial mass, amount of UCP1 protein, and thermogenic capacity. Importantly, mitochondria are widely known as a therapeutic target of melatonin; however, direct evidence of melatonin on the function of mitochondria from BAT and the mechanistic pathways underlying these effects remains lacking. This study investigated the effects of melatonin on mitochondrial functions in BAT of Zücker diabetic fatty (ZDF) rats, which are considered a model of obesity-related type 2 diabetes mellitus (T2DM). At five weeks of age, Zücker lean (ZL) and ZDF rats were subdivided into two groups, consisting of control and treated with oral melatonin for six weeks. Mitochondria were isolated from BAT of animals from both groups, using subcellular fractionation techniques, followed by measurement of several mitochondrial parameters, including respiratory control ratio (RCR), phosphorylation coefficient (ADP/O ratio), ATP production, level of mitochondrial nitrites, superoxide dismutase activity, and alteration in the mitochondrial permeability transition pore (mPTP). Interestingly, melatonin increased RCR in mitochondria from brown fat of both ZL and ZDF rats through the reduction of the proton leak component of respiration (state 4). In addition, melatonin improved the ADP/O ratio in obese rats and augmented ATP production in lean rats. Further, melatonin reduced mitochondrial nitrosative and oxidative status by decreasing nitrite levels and increasing superoxide dismutase activity in both groups, as well as inhibited mPTP in mitochondria isolated from brown fat. Taken together, the present data revealed that chronic oral administration of melatonin improved mitochondrial respiration in brown adipocytes, while decreasing oxidative and nitrosative stress and susceptibility of adipocytes to apoptosis in ZDF rats, suggesting a beneficial use in the treatment of diabesity. Further research regarding the molecular mechanisms underlying the effects of melatonin on diabesity is warranted. Full article

(This article belongs to the Special Issue Mitochondrial Dysfunction and Oxidative Stress in Diabetes and Associated Diseases)

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Figure 1

Figure 1
The effect of melatonin treatment on respiratory states in isolated mitochondria from brown fat depots of control (untreated) and melatonin-treated ZDF and ZL rats. (A) The upper panel shows state 3, representing oxygen flux, while producing ATP in response to ADP pulses in the presence of substrates. (B) The lower panel illustrates state 4, or leak respiration, which shows oxygen flux in the absence of ATP synthesis. Glutamate/malate was used as the respiratory substrates. C, control; M, melatonin; ZL, Zücker lean rats; ZDF, Zücker diabetic fatty rats. Values are shown as mean ± SD. Superscript characters show significant differences determined by two-way analysis of variance (ANOVA) followed by the Tukey post hoc test (** p < 0.01, M-ZDF compared with C-ZDF rats; # p < 0.05, C-ZDF compared with C-ZL rats). Full article ">Figure 2
Respiratory control ratio (RCR) of mitochondria isolated from brown adipose fat depots of control (untreated) and melatonin-treated ZDF and ZL rats. RCR was defined as the ratio of state 3 to state 4. Data are shown as mean ± SD. ZL, Zücker lean rats; ZDF, Zücker diabetic fatty rats. Superscript characters indicate significant differences determined by two-way ANOVA followed by the Tukey post hoc test (** p < 0.01, M-ZDF compared with C-ZDF and M-ZL compared with C-ZL animals; ## p < 0.01, C-ZDF and M-ZDF compared with C-ZL rats). Full article ">Figure 3
Respiratory phosphorylation coefficient (ADP/O ratio) of brown adipose tissue (BAT)-isolated mitochondria from control (untreated) and melatonin-treated ZDF and ZL rats. Values are shown as mean ± SD. Superscript characters show significant differences determined by two-way ANOVA followed by the Tukey post hoc test (** p < 0.01, M-ZDF compared with C-ZDF rats; ## p < 0.01, C-ZDF and M-ZDF compared with C-ZL rats). Full article ">Figure 4
ATP levels of BAT-isolated mitochondria of different treated groups. Data were normalized for variations in mitochondrial content in an equivalent amount of tissue (micrograms of ATP/mg of tissue wet weight), adjusted to 0.5 mg/mL protein concentration, and expressed as nmol/mg protein. Data are shown as mean ± SD. Superscript characters show significant differences determined by two-way ANOVA followed by the Tukey post hoc test (* p < 0.01, M-ZL compared with C-ZL rats; # p < 0.05, C-ZDF compared with C-ZL rats). Full article ">Figure 5
The effect of melatonin on nitrite levels in mitochondria isolated from BAT fat depots of control (untreated) and melatonin-treated ZDF and ZL rats. Values are shown as mean ± SD. Superscript letters express significant difference measured using two-way ANOVA followed by the Tukey post hoc test. * p < 0.05 (M-ZL compared with C-ZL rats), ** p < 0.01 (M-ZDF compared with C-ZDF rats), and # p < 0.05 (C-ZDF and M-ZDF compared with C-ZL rats). Full article ">Figure 6
The effect of melatonin treatment on superoxide dismutase (SOD) activity in mitochondria isolated from BAT of control (untreated) and melatonin-treated ZDF and ZL rats. Values are expressed as mean ± SD. Superscript letters identify significant difference measured using two-way ANOVA followed by the Tukey post hoc test. ZL, Zücker lean rats; ZDF, Zücker diabetic fatty rats. ** p < 0.01, M-ZDF compared with C-ZDF rats and M-ZL compared with C-ZL animals. Full article ">Figure 7
The effect of melatonin treatment on calcium-induced permeability transition pore (PTP) in mitochondria isolated from BAT of control (untreated) and melatonin-treated ZDF and ZL rats. The effect of cyclosporine A (CsA) was included as a classical inhibitor of mitochondrial PTP. Data are shown as mean ± SD of the area under the curve (AUC). Superscript letters identify significant difference measured using two-way ANOVA followed by the Tukey post hoc test. ZL, Zücker lean rats; ZDF, Zücker diabetic fatty rats. *** p < 0.001 and # p < 0.05. Full article ">

27 pages, 5119 KiB

Open AccessArticle

Sirt1 and Sirt3 Activation Improved Cardiac Function of Diabetic Rats via Modulation of Mitochondrial Function

by Bugga Paramesha, Mohammed Soheb Anwar, Himanshu Meghwani, Subir Kumar Maulik, Sudheer Kumar Arava and Sanjay K Banerjee

Antioxidants 2021, 10(3), 338; https://doi.org/10.3390/antiox10030338 - 24 Feb 2021

Cited by 21 | Viewed by 4746

Abstract

In the present study, we aimed to evaluate the effect of Sirt1, Sirt3 and combined activation in high fructose diet-induced insulin resistance rat heart and assessed the cardiac function focusing on mitochondrial health and function. We administered the Sirt1 activator; SRT1720 (5 mg/kg, i.p.), Sirt3 activator; Oroxylin-A (10 mg/kg i.p.) and the combination; SRT1720 + Oroxylin-A (5 mg/kg and 10 mg/kg i.p.) daily from 12th week to 20th weeks of study. We observed significant perturbations of most of the cardiac structural and functional parameters in high fructose diet-fed animals. Administration of SRT1720 and Oroxylin-A improved perturbed cardiac structural and functional parameters by decreasing insulin resistance, oxidative stress, and improving mitochondrial function by enhancing mitochondrial biogenesis, OXPHOS expression and activity in high fructose diet-induced insulin-resistant rats. However, we could not observe the synergistic effect of SRT1720 and Oroxylin-A combination. Similar to in-vivo study, perturbed mitochondrial function and oxidative stress observed in insulin-resistant H9c2 cells were improved after activation of Sirt1 and Sirt3. We observed that Sirt1 activation enhances Sirt3 expression and mitochondrial biogenesis, and the opposite effects were observed after Sirt1 inhibition in cardiomyoblast cells. Taken together our results conclude that activation of Sirt1 alone could be a potential therapeutic target for diabetes-associated cardiovascular complications. Full article

(This article belongs to the Special Issue Mitochondrial Dysfunction and Oxidative Stress in Diabetes and Associated Diseases)

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15 pages, 2013 KiB

Open AccessArticle

Effects of Apocynin on Heart Muscle Oxidative Stress of Rats with Experimental Diabetes: Implications for Mitochondria

by Estefanía Bravo-Sánchez, Donovan Peña-Montes, Sarai Sánchez-Duarte, Alfredo Saavedra-Molina, Elizabeth Sánchez-Duarte and Rocío Montoya-Pérez

Antioxidants 2021, 10(3), 335; https://doi.org/10.3390/antiox10030335 - 24 Feb 2021

Cited by 12 | Viewed by 2754

Abstract

Diabetes mellitus (DM) constitutes one of the public health problems today. It is characterized by hyperglycemia through a defect in the ?-cells function and/or decreased insulin sensitivity. Apocynin has been tasted acting directly as an NADPH oxidase inhibitor and reactive oxygen species (ROS) scavenger, exhibiting beneficial effects against diabetic complications. Hence, the present study’s goal was to dissect the possible mechanisms by which apocynin could mediate its cardioprotective effect against DM-induced oxidative stress. Male Wistar rats were assigned into 4 groups: Control (C), control + apocynin (C+A), diabetes (D), diabetes + apocynin (D+A). DM was induced with streptozotocin. Apocynin treatment (3 mg/kg/day) was applied for 5 weeks. Treatment significantly decreased blood glucose levels and insulin resistance in diabetic rats. In cardiac tissue, ROS levels were higher, and catalase enzyme activity was reduced in the D group compared to the C group; the apocynin treatment significantly attenuated these responses. In heart mitochondria, Complexes I and II of the electron transport chain (ETC) were significantly enhanced in the D+A group. Total glutathione, the level of reduced glutathione (GSH) and the GSH/ oxidized glutathione (GSSG) ratio were increased in the D+A group. Superoxide dismutase (SOD) and the glutathione peroxidase (GSH-Px) activities were without change. Apocynin enhances glucose uptake and insulin sensitivity, preserving the antioxidant defense and mitochondrial function. Full article

(This article belongs to the Special Issue Mitochondrial Dysfunction and Oxidative Stress in Diabetes and Associated Diseases)

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Figure 1

Figure 1
Effect of Apocynin on metabolic biomarkers. This figure shows bodyweight of the different groups of rats (a) (g); fasting glucose levels (b) (mg/dL); postprandrial glucose levels (c) (mg/dL); glucose levels in the insulin-tolerance test (ITT) (d) (mg/dL); area under the curve (e) (mg/dL/min); glucose disappearance rate (KITT) during the ITT (f) (%/min). C = control; A = apocynin; D = diabetic; D+A = diabetic + apocynin. n = 6. Data are presented as the mean ± standard error. (2-way ANOVA, Tukey post-hoc test). The different letters (lower case) indicate the significant differences between groups with p < 0.05. Full article ">Figure 2
Levels of Reactive Oxygen Species in the heart of different groups of rats. This figure shows the Reactive Oxygen Species (ΔF) levels in the heart for each group C = control, A = apocynin, D = diabetic, D+A = diabetic + apocynin. n = 6; Data are presented as the mean ± standard error (One-way ANOVA, Tukey posthoc test). The different letters indicate the significant differences between groups, with p < 0.05. Full article ">Figure 3
Catalase enzyme activity in the heart of different groups. This figure shows the catalase enzyme activity (U of activity/mg of prot) in the heart for each group C = control, A = apocynin, D = diabetic, D+A = diabetic + apocynin. n = 6. Data are presented as the mean ± standard error (One-way ANOVA, Tukey posthoc test). The different letters indicate the significant differences between groups, with p < 0.05. Full article ">Figure 4
Effect of apocynin on enzymatic activities of complexes of the electron transport chain (ETC) in heart mitochondria. (a) Complex I activity. (b) Complex II activity. (c) Complexes II–III. (d) Complex IV. Different letters indicate significant differences between groups, ns: Not significant, (p ≤ 0.05) by one-way ANOVA with Tukey post hoc test. Values represent means ± SEM. Control group, C, normoglycemic + apocynin group, A, diabetic group, D, and diabetic + apocynin group, D+A. Full article ">Figure 5
Effect of apocynin on oxidative stress in heart mitochondria. (a) Total glutathione. (b) Oxidized glutathione. (c) Reduced glutathione. (d) GSH/GSSG ratio. (e) SOD activity. (f) GSH-Px activity. Different letters indicate significant differences between groups; ns: Not significant (p ≤ 0.05) by one-way ANOVA with Tukey post hoc test. Values represent means ± SEM. Control group, C, normoglycemic + apocynin group, A, diabetic group, D, and diabetic + apocynin group, D+A. Full article ">

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19 pages, 1214 KiB

Open AccessReview

Role of Oxidative Stress in Diabetic Cardiomyopathy

by Bart De Geest and Mudit Mishra

Antioxidants 2022, 11(4), 784; https://doi.org/10.3390/antiox11040784 - 15 Apr 2022

Cited by 82 | Viewed by 7539

Abstract

Type 2 diabetes is a redox disease. Oxidative stress and chronic inflammation induce a switch of metabolic homeostatic set points, leading to glucose intolerance. Several diabetes-specific mechanisms contribute to prominent oxidative distress in the heart, resulting in the development of diabetic cardiomyopathy. Mitochondrial overproduction of reactive oxygen species in diabetic subjects is not only caused by intracellular hyperglycemia in the microvasculature but is also the result of increased fatty oxidation and lipotoxicity in cardiomyocytes. Mitochondrial overproduction of superoxide anion radicals induces, via inhibition of glyceraldehyde 3-phosphate dehydrogenase, an increased polyol pathway flux, increased formation of advanced glycation end-products (AGE) and activation of the receptor for AGE (RAGE), activation of protein kinase C isoforms, and an increased hexosamine pathway flux. These pathways not only directly contribute to diabetic cardiomyopathy but are themselves a source of additional reactive oxygen species. Reactive oxygen species and oxidative distress lead to cell dysfunction and cellular injury not only via protein oxidation, lipid peroxidation, DNA damage, and oxidative changes in microRNAs but also via activation of stress-sensitive pathways and redox regulation. Investigations in animal models of diabetic cardiomyopathy have consistently demonstrated that increased expression of the primary antioxidant enzymes attenuates myocardial pathology and improves cardiac function. Full article

(This article belongs to the Special Issue Mitochondrial Dysfunction and Oxidative Stress in Diabetes and Associated Diseases)

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23 pages, 1401 KiB

Open AccessReview

Mitochondrial Uncoupling Proteins (UCPs) as Key Modulators of ROS Homeostasis: A Crosstalk between Diabesity and Male Infertility?

by Bruno S. Monteiro, Laís Freire-Brito, David F. Carrageta, Pedro F. Oliveira and Marco G. Alves

Antioxidants 2021, 10(11), 1746; https://doi.org/10.3390/antiox10111746 - 30 Oct 2021

Cited by 25 | Viewed by 6413

Abstract

Uncoupling proteins (UCPs) are transmembrane proteins members of the mitochondrial anion transporter family present in the mitochondrial inner membrane. Currently, six homologs have been identified (UCP1-6) in mammals, with ubiquitous tissue distribution and multiple physiological functions. UCPs are regulators of key events for cellular bioenergetic metabolism, such as membrane potential, metabolic efficiency, and energy dissipation also functioning as pivotal modulators of ROS production and general cellular redox state. UCPs can act as proton channels, leading to proton re-entry the mitochondrial matrix from the intermembrane space and thus collapsing the proton gradient and decreasing the membrane potential. Each homolog exhibits its specific functions, from thermogenesis to regulation of ROS production. The expression and function of UCPs are intimately linked to diabesity, with their dysregulation/dysfunction not only associated to diabesity onset, but also by exacerbating oxidative stress-related damage. Male infertility is one of the most overlooked diabesity-related comorbidities, where high oxidative stress takes a major role. In this review, we discuss in detail the expression and function of the different UCP homologs. In addition, the role of UCPs as key regulators of ROS production and redox homeostasis, as well as their influence on the pathophysiology of diabesity and potential role on diabesity-induced male infertility is debated. Full article

(This article belongs to the Special Issue Mitochondrial Dysfunction and Oxidative Stress in Diabetes and Associated Diseases)

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Figure 1
Proton transport and formation of ROS during oxidative phosphorylation. (A) In complex I, the oxidation of NADH (generated through glycolysis, β-oxidation, and Krebs cycle) to NAD+ transfers two electrons to the complex. Complex I will then transfer the electrons to the quinone reservoir by reducing ubiquinone to ubiquinol. In complex II occurs the oxidation of succinate to fumarate, a reaction that reduces FAD to FADH2. FADH2 also gives two electrons to ubiquinone, originating FAD and ubiquinol. Ubiquinol is released into the quinone reservoir, joining those from NADH. Ubiquinol transports electrons trough the intermembrane space to complex III, where they are again oxidized to quinones. Complex III transfers electrons to cytochrome c, which moves to complex IV. Complex IV receives the electrons from cytochrome c and transfers them to molecular oxygen, reducing it to water. Same electrons escape to oxygen, which lead to the formation of superoxide anions. Superoxide leads to a cascade of redox reactions, which leads to the formation of other ROS, such as the hydroxyl radical (•OH) and hydrogen peroxide (H2O2). During the transport of electrons through the respiratory chain, protons are pumped from the matrix into the intermembrane space by complexes I, II, and IV. This action creates an electrochemical gradient that is used to (B) convert ADP into ATP, by ATP synthase. The proton transport to the mitochondrial matrix can be also made through (C) basal proton leak or (D) inducible proton leak. Full article ">Figure 2
Molecular structure and hypothesized models for proton transport by UCPs. (A) UCPs are constituted by three repetition domains, each composed of two α-helix regions. (B) The proposed models for proton transport by UCPs are (a) flip-flop model; (b) cofactor model (transport linked to fatty acids); (c) cofactor model (independent transport). Full article ">

28 pages, 1873 KiB

Open AccessReview

Diabetes and Alzheimer’s Disease: Might Mitochondrial Dysfunction Help Deciphering the Common Path?

by Maria Assunta Potenza, Luca Sgarra, Vanessa Desantis, Carmela Nacci and Monica Montagnani

Antioxidants 2021, 10(8), 1257; https://doi.org/10.3390/antiox10081257 - 6 Aug 2021

Cited by 36 | Viewed by 8610

Abstract

A growing number of clinical and epidemiological studies support the hypothesis of a tight correlation between type 2 diabetes mellitus (T2DM) and the development risk of Alzheimer’s disease (AD). Indeed, the proposed definition of Alzheimer’s disease as type 3 diabetes (T3D) underlines the key role played by deranged insulin signaling to accumulation of aggregated amyloid beta (A?) peptides in the senile plaques of the brain. Metabolic disturbances such as hyperglycemia, peripheral hyperinsulinemia, dysregulated lipid metabolism, and chronic inflammation associated with T2DM are responsible for an inefficient transport of insulin to the brain, producing a neuronal insulin resistance that triggers an enhanced production and deposition of A? and concomitantly contributes to impairment in the micro-tubule-associated protein Tau, leading to neural degeneration and cognitive decline. Furthermore, the reduced antioxidant capacity observed in T2DM patients, together with the impairment of cerebral glucose metabolism and the decreased performance of mitochondrial activity, suggests the existence of a relationship between oxidative damage, mitochondrial impairment, and cognitive dysfunction that could further reinforce the common pathophysiology of T2DM and AD. In this review, we discuss the molecular mechanisms by which insulin-signaling dysregulation in T2DM can contribute to the pathogenesis and progression of AD, deepening the analysis of complex mechanisms involved in reactive oxygen species (ROS) production under oxidative stress and their possible influence in AD and T2DM. In addition, the role of current therapies as tools for prevention or treatment of damage induced by oxidative stress in T2DM and AD will be debated. Full article

(This article belongs to the Special Issue Mitochondrial Dysfunction and Oxidative Stress in Diabetes and Associated Diseases)

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