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Related Concept Videos

Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
Psychoneuroimmunology: Diabetes and Cancer01:19

Psychoneuroimmunology: Diabetes and Cancer

Chronic stress has been linked to both the onset and progression of serious health conditions, including Type 2 diabetes and cancer. Type 2 diabetes, a widespread chronic illness, is closely associated with obesity and insulin resistance, both of which often worsen under stress. Studies indicate that men experiencing high levels of chronic stress face a 45% higher risk of developing diabetes compared to those with minimal stress. Stress triggers physiological responses that elevate blood...
Diabetic Neuropathy01:22

Diabetic Neuropathy

DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
Diabetic Retinopathy01:27

Diabetic Retinopathy

DefinitionDiabetic retinopathy is a microvascular complication of diabetes affecting the retinal blood vessels.Risk FactorsDiabetic retinopathy is present in almost all individuals with type 1 diabetes and more than 60% of those with type 2 diabetes after two decades of disease.The risk increases with poor glycemic control, hypertension, dyslipidemia, smoking, pregnancy, and puberty.Although cataracts and glaucoma are also more frequent in people with diabetes, retinopathy remains the leading...

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Related Experiment Video

Updated: May 14, 2026

Quantification of Reactive Oxygen Species Using 2′,7′-Dichlorofluorescein Diacetate Probe and Flow-Cytometry in Müller Glial Cells
14:25

Quantification of Reactive Oxygen Species Using 2′,7′-Dichlorofluorescein Diacetate Probe and Flow-Cytometry in Müller Glial Cells

Published on: May 13, 2022

Oxidative stress in diabetes.

Krisztian Stadler1

  • 1Pennington Biomedical Research Center, Baton Rouge, Louisiana, USA. krisztian.stadler@pbrc.edu

Advances in Experimental Medicine and Biology
|February 9, 2013
PubMed
Summary

Oxidative stress contributes to diabetes (Type 1 and Type 2) and related conditions. Understanding redox imbalance mechanisms is crucial for developing effective clinical interventions for these widespread diseases.

Area of Science:

  • Endocrinology and Metabolism
  • Molecular Biology
  • Pathophysiology

Background:

  • Diabetes, obesity, and metabolic syndrome are at epidemic levels globally.
  • Oxidative stress and redox imbalance are implicated in the pathology and progression of diabetes.
  • Understanding molecular mechanisms is vital for clinical intervention.

Purpose of the Study:

  • To review the latest knowledge on oxidative stress in diabetes.
  • To discuss current evidence and ongoing debates regarding redox imbalance in diabetes.
  • To highlight the role of oxidative stress in Type 1 and Type 2 diabetes.

Main Methods:

  • Literature review of recent studies on oxidative stress and diabetes.
  • Analysis of molecular and cellular mechanisms of redox imbalance.

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Published on: June 25, 2018

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Last Updated: May 14, 2026

Quantification of Reactive Oxygen Species Using 2′,7′-Dichlorofluorescein Diacetate Probe and Flow-Cytometry in Müller Glial Cells
14:25

Quantification of Reactive Oxygen Species Using 2′,7′-Dichlorofluorescein Diacetate Probe and Flow-Cytometry in Müller Glial Cells

Published on: May 13, 2022

A Murine Pancreatic Islet Cell-based Screening for Diabetogenic Environmental Chemicals
07:39

A Murine Pancreatic Islet Cell-based Screening for Diabetogenic Environmental Chemicals

Published on: June 25, 2018

  • Synthesis of current evidence and identification of key research questions.
  • Main Results:

    • Extensive research links oxidative stress to diabetes pathogenesis.
    • Redox imbalance plays a significant role at cellular and subcellular levels.
    • Current studies offer new insights into disease mechanisms.

    Conclusions:

    • Oxidative stress is a critical factor in diabetes development and progression.
    • Further research into redox mechanisms can guide therapeutic strategies.
    • Addressing oxidative stress is essential for managing diabetes epidemics.