scholarly journals Relationship Between Oxidative Stress, ER Stress, and Inflammation in Type 2 Diabetes: The Battle Continues

2019 ◽  
Vol 8 (9) ◽  
pp. 1385 ◽  
Author(s):  
Burgos-Morón ◽  
Abad-Jiménez ◽  
Marañón ◽  
Iannantuoni ◽  
Escribano-López ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Er Stress ◽  
Mitochondrial Dysfunction ◽  
Current Knowledge ◽  
Β Cells ◽  
The Relationship ◽  
And Oxidative Stress

Type 2 diabetes (T2D) is a metabolic disorder characterized by hyperglycemia and insulin resistance in which oxidative stress is thought to be a primary cause. Considering that mitochondria are the main source of ROS, we have set out to provide a general overview on how oxidative stress is generated and related to T2D. Enhanced generation of reactive oxygen species (ROS) and oxidative stress occurs in mitochondria as a consequence of an overload of glucose and oxidative phosphorylation. Endoplasmic reticulum (ER) stress plays an important role in oxidative stress, as it is also a source of ROS. The tight interconnection between both organelles through mitochondrial-associated membranes (MAMs) means that the ROS generated in mitochondria promote ER stress. Therefore, a state of stress and mitochondrial dysfunction are consequences of this vicious cycle. The implication of mitochondria in insulin release and the exposure of pancreatic β-cells to hyperglycemia make them especially susceptible to oxidative stress and mitochondrial dysfunction. In fact, crosstalk between both mechanisms is related with alterations in glucose homeostasis and can lead to the diabetes-associated insulin-resistance status. In the present review, we discuss the current knowledge of the relationship between oxidative stress, mitochondria, ER stress, inflammation, and lipotoxicity in T2D.

scholarly journals MicroRNAs and Oxidative Stress: An Intriguing Crosstalk to Be Exploited in the Management of Type 2 Diabetes

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 802
Author(s):  
Teresa Vezza ◽  
Aranzazu M. de Marañón ◽  
Francisco Canet ◽  
Pedro Díaz-Pozo ◽  
Miguel Marti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Signaling Pathways ◽  
Current Knowledge ◽  
Critical Role ◽  
Cell Dysfunction ◽  
Non Coding Rnas ◽  
And Oxidative Stress ◽  
Molecular Crosstalk

Type 2 diabetes is a chronic disease widespread throughout the world, with significant human, social, and economic costs. Its multifactorial etiology leads to persistent hyperglycemia, impaired carbohydrate and fat metabolism, chronic inflammation, and defects in insulin secretion or insulin action, or both. Emerging evidence reveals that oxidative stress has a critical role in the development of type 2 diabetes. Overproduction of reactive oxygen species can promote an imbalance between the production and neutralization of antioxidant defence systems, thus favoring lipid accumulation, cellular stress, and the activation of cytosolic signaling pathways, and inducing β-cell dysfunction, insulin resistance, and tissue inflammation. Over the last few years, microRNAs (miRNAs) have attracted growing attention as important mediators of diverse aspects of oxidative stress. These small endogenous non-coding RNAs of 19–24 nucleotides act as negative regulators of gene expression, including the modulation of redox signaling pathways. The present review aims to provide an overview of the current knowledge concerning the molecular crosstalk that takes place between oxidative stress and microRNAs in the physiopathology of type 2 diabetes, with a special emphasis on its potential as a therapeutic target.

scholarly journals Lipotoxicity and β-Cell Failure in Type 2 Diabetes: Oxidative Stress Linked to NADPH Oxidase and ER Stress

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3328
Author(s):  
Eloisa Aparecida Vilas-Boas ◽  
Davidson Correa Almeida ◽  
Leticia Prates Roma ◽  
Fernanda Ortis ◽  
Angelo Rafael Carpinelli
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Nadph Oxidase ◽  
Er Stress ◽  
Cell Function ◽  
Caloric Intake ◽  
Β Cells ◽  
Β Cell ◽  
Β Cell Function

A high caloric intake, rich in saturated fats, greatly contributes to the development of obesity, which is the leading risk factor for type 2 diabetes (T2D). A persistent caloric surplus increases plasma levels of fatty acids (FAs), especially saturated ones, which were shown to negatively impact pancreatic β-cell function and survival in a process called lipotoxicity. Lipotoxicity in β-cells activates different stress pathways, culminating in β-cells dysfunction and death. Among all stresses, endoplasmic reticulum (ER) stress and oxidative stress have been shown to be strongly correlated. One main source of oxidative stress in pancreatic β-cells appears to be the reactive oxygen species producer NADPH oxidase (NOX) enzyme, which has a role in the glucose-stimulated insulin secretion and in the β-cell demise during both T1 and T2D. In this review, we focus on the acute and chronic effects of FAs and the lipotoxicity-induced β-cell failure during T2D development, with special emphasis on the oxidative stress induced by NOX, the ER stress, and the crosstalk between NOX and ER stress.

Taurine ameliorates mitochondrial dysfunction and oxidative stress in the heart of rats with type 2 diabetes

2016 ◽  
Vol 42 (4) ◽  
pp. 294 ◽  
Author(s):  
Nataliia Gorbenko ◽  
Oleksiy Borikov ◽  
Olga Ivanova ◽  
Tatiana Zvyagina ◽  
Katerina Taran ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Mitochondrial Dysfunction ◽  
And Oxidative Stress

scholarly journals Designing a late-stage type 2 diabetes mellitus model with brain insulin resistance and oxidative stress

2021 ◽  
Author(s):  
Rocío Redondo-Castillejo ◽  
Marina Hernández-Martín ◽  
Luis García-García ◽  
Juana Benedí ◽  
Adrián Macho-González ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Late Stage ◽  
Brain Insulin ◽  
Brain Insulin Resistance ◽  
And Oxidative Stress

scholarly journals Relationship between 25 Hydroxyvitamin D, Overweight/Obesity Status, Pro-Inflammatory and Oxidative Stress Markers in Patients with Type 2 Diabetes: A Simplified Empirical Path Model

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2889
Author(s):  
Adriana Florinela Cӑtoi ◽  
Mihaela Iancu ◽  
Alina Elena Pârvu ◽  
Andra Diana Cecan ◽  
Cristina Bidian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Vitamin D ◽  
Systemic Inflammation ◽  
Hydroxyvitamin D ◽  
Obesity Status ◽  
25 Hydroxyvitamin D ◽  
And Oxidative Stress

Vitamin D deficiency is highly prevalent in patients with overweight/obesity and type 2 diabetes (T2DM). Herein, we investigated the relationship between vitamin D status and overweight/obesity status, insulin resistance (IR), systemic inflammation as well as oxidative stress (OS). Anthropometric and laboratory assessments of 25-hydroxyvitamin D (25(OH)D) and glycemic, pro-inflammatory and OS biomarkers were performed in a sample of 47 patients with T2DM who were divided into categories based on overweight and degree of obesity. The main findings were: the overweight/obesity status correlated negatively with the degree of serum 25(OH)D deficiency (ρ = −0.27) with a trend towards statistical significance (p = 0.069); the homeostasis model assessment of insulin resistance (HOMA-IR) was significantly different (p = 0.024) in patients with 25(OH)D deficiency, as was total oxidant status (TOS) and oxidative stress index (OSI) in patients with severe serum 25(OH)D deficiency as compared to those with 25(OH)D over 20 ng/mL (TOS: p = 0.007, OSI: p = 0.008); and 25(OH)D had a negative indirect effect on TOS by body mass index (BMI), but BMI was not a significant mediator of the studied relationship. In a setting of overweight and increasing degree of obesity, patients with T2DM did not display decreasing values of 25(OH)D. Subjects with the lowest values of 25(OH)D presented the highest values of BMI. Patients with 25(OH)D deficiency were more insulin resistant and showed increased OS but no elevated systemic inflammation. The negative effect of 25(OH)D on TOS did not seem to involve BMI as a mediator.

The sensitivity of pancreatic β-cells to mitochondrial injuries triggered by lipotoxicity and oxidative stress

2008 ◽  
Vol 36 (5) ◽  
pp. 930-934 ◽  
Author(s):  
Ning Li ◽  
Francesca Frigerio ◽  
Pierre Maechler
Keyword(s):  
Oxidative Stress ◽  
Current Knowledge ◽  
Β Cells ◽  
Β Cell ◽  
Pancreatic Β Cells ◽  
Primary Target ◽  
Glucose Homoeostasis ◽  
Insulin Secreting Cells ◽  
And Oxidative Stress

Pancreatic β-cells are essential for the maintenance of glucose homoeostasis, and dysfunction of these insulin-secreting cells results in the development of diabetes. In the course of events leading from obesity to Type 2 diabetes, several mechanisms are currently envisaged. Among them, lipids and oxidative stress are considered as toxic candidates for the β-cell. The cellular link between fatty acids and ROS (reactive oxygen species) is essentially the mitochondrion, a key organelle for the control of insulin secretion. Mitochondria are the main source of ROS and are also the primary target of oxidative attacks. The present review presents the current knowledge of lipotoxicity related to oxidative stress in the context of mitochondrial function in the β-cell.

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