Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

75
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...
75
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

28
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.
28
Pathophysiology of Diabetes01:20

Pathophysiology of Diabetes

3.9K
Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility,...
3.9K
Diabetes Mellitus: Overview and Type I Subtype01:22

Diabetes Mellitus: Overview and Type I Subtype

5.5K
Diabetes mellitus is a chronic metabolic disorder characterized by high blood glucose levels due to inadequate insulin production, insulin resistance, or both. The condition affects millions worldwide and can significantly impact their health and quality of life.
Type 1 diabetes is an autoimmune disease in which the immune system mistakenly attacks and destroys the insulin-producing beta cells in the pancreas. As a result, the body is unable to produce sufficient insulin, and individuals with...
5.5K
Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

17
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...
17
Type I Diabetes I: Introduction01:12

Type I Diabetes I: Introduction

45
Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1...
45

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Evidence for the Collective Nature of Radial Flow in Pb+Pb Collisions with the ATLAS Detector.

Physical review letters·2026
Same author

Evidence for the Dimuon Decay of the Higgs Boson in pp Collisions with the ATLAS Detector.

Physical review letters·2025
Same author

Evidence for Longitudinally Polarized W Bosons in the Electroweak Production of Same-Sign W Boson Pairs in Association with Two Jets in pp Collisions at sqrt[s]=13  TeV with the ATLAS Detector.

Physical review letters·2025
Same author

Observation of tt[over ¯] Production in Pb+Pb Collisions at sqrt[s_{NN}]=5.02  TeV with the ATLAS Detector.

Physical review letters·2025
Same author

Search for Dark Matter Produced in Association with a Dark Higgs Boson in the bb[over ¯] Final State Using pp Collisions at sqrt[s]=13  TeV with the ATLAS Detector.

Physical review letters·2025
Same author

Search for Magnetic Monopole Pair Production in Ultraperipheral Pb+Pb Collisions at sqrt[s_{NN}]=5.36  TeV with the ATLAS Detector at the LHC.

Physical review letters·2025

Related Experiment Video

Updated: May 3, 2026

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test OGTT and Insulin Tolerance Test ITT
08:13

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test OGTT and Insulin Tolerance Test ITT

Published on: January 7, 2018

70.1K

Iron: the hard player in diabetes pathophysiology.

J B Hansen1, I W Moen, T Mandrup-Poulsen

  • 1Section for Endocrinological Research, Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark; Department of Physiology, University of Toronto, Toronto, ON, Canada.

Acta Physiologica (Oxford, England)
|February 14, 2014
PubMed
Summary

Iron overload contributes to diabetes by causing pancreatic islet inflammation and cell death through oxidative stress. Iron chelation may offer a therapeutic strategy for diabetes, pending clinical trials.

Keywords:
inflammationiron transportmitochondrial stressoxidative stressreactive oxygen speciesβ-cell

More Related Videos

Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model
06:22

Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model

Published on: November 29, 2024

1.7K
Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
09:40

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Published on: January 19, 2017

10.8K

Related Experiment Videos

Last Updated: May 3, 2026

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test OGTT and Insulin Tolerance Test ITT
08:13

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test OGTT and Insulin Tolerance Test ITT

Published on: January 7, 2018

70.1K
Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model
06:22

Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model

Published on: November 29, 2024

1.7K
Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
09:40

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Published on: January 19, 2017

10.8K

Area of Science:

  • Endocrinology
  • Metabolic Disease Research
  • Cellular Biology

Background:

  • Recent evidence highlights iron's critical role in diabetes pathophysiology, influencing pancreatic islet inflammation and serving as a biomarker for diabetes risk.
  • Iron metabolism in pancreatic beta cells is complex, with excess iron being toxic yet essential for normal function and glucose homeostasis.

Purpose of the Study:

  • To review and discuss current evidence implicating iron as a key pathogenic factor in both type 1 and type 2 diabetes.
  • To focus on the role of inflammatory pathways in iron-mediated beta-cell damage.

Main Methods:

  • Review of recent scientific literature on iron metabolism, diabetes, inflammation, and oxidative stress.
  • Analysis of proposed mechanisms linking pro-inflammatory cytokines, iron uptake, and beta-cell apoptosis.

Main Results:

  • Iron generates reactive oxygen species (ROS) via Fenton chemistry, leading to oxidative damage and apoptosis in beta cells.
  • Pro-inflammatory cytokine IL-1β enhances beta-cell iron uptake via DMT1, promoting ROS formation and apoptosis, linking inflammation to oxidative damage.
  • Iron-induced ROS may contribute to beta-cell dedifferentiation and death through various cellular pathways.

Conclusions:

  • Iron plays a significant role in the pathogenesis of both type 1 and type 2 diabetes, particularly through inflammatory pathways.
  • Iron chelation presents a potential therapeutic avenue for reducing diabetes severity and mortality.
  • Further clinical trials are necessary to evaluate the efficacy and safety of iron reduction therapies in diabetes management.