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Related Concept Videos

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 I Diabetes I: Introduction01:12

Type I Diabetes I: Introduction

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 diabetes is an...
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.
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...
Diabetes Mellitus: Overview and Type I Subtype01:22

Diabetes Mellitus: Overview and Type I Subtype

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...
Diabetes Mellitus: Type 2 and Gestational01:22

Diabetes Mellitus: Type 2 and Gestational

Type 2 diabetes, characterized by insulin resistance, arises when the insulin receptors on cells lose responsiveness to insulin, diminishing the cell's capacity to take up glucose, resulting in elevated blood glucose levels. To receive a diagnosis of Type 2 diabetes, a series of blood glucose tests are necessary to assess whether the blood glucose falls within normal parameters. If the result is out of the normal range, a patient may be diagnosed as prediabetic or diabetic, depending on the...

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Updated: May 7, 2026

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
06:27

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells

Published on: May 6, 2013

Do post-translational beta cell protein modifications trigger type 1 diabetes?

Joachim Størling1, Anne Julie Overgaard, Caroline Anna Brorsson

  • 1Copenhagen Diabetes Research Center (DIRECT), Herlev University Hospital, Herlev Ringvej 75, 2730, Herlev, Denmark, joachim.stoerling.01@regionh.dk.

Diabetologia
|September 20, 2013
PubMed
Summary
This summary is machine-generated.

Type 1 diabetes may not be a classical autoimmune disease. Modified beta cell proteins, not native ones, might trigger the immune response and beta cell destruction.

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Last Updated: May 7, 2026

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Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes
12:12

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes

Published on: June 16, 2011

Area of Science:

  • Immunology
  • Endocrinology
  • Genetics

Background:

  • Type 1 diabetes involves T cell destruction of insulin-producing beta cells.
  • No beta cell-specific antigens have been identified besides insulin.
  • Post-translational modifications (PTMs) create neo-epitopes in other autoimmune diseases.

Purpose of the Study:

  • To investigate the role of PTMs in creating beta cell-specific neo-epitopes in Type 1 diabetes.
  • To propose a modified model for Type 1 diabetes pathogenesis.
  • To re-evaluate the classification of Type 1 diabetes as a classical autoimmune disease.

Main Methods:

  • Literature review of PTM involvement in autoimmune diseases.
  • Genetic analysis of Type 1 diabetes-associated polymorphisms.
  • Human islet gene expression analysis following cytokine treatment.

Main Results:

  • Evidence suggests PTMs create neo-epitopes on beta cell proteins.
  • Cytokines alter gene expression of PTM-related proteins in human islets.
  • Type 1 diabetes-associated polymorphisms exist in genes involved in PTM.

Conclusions:

  • PTMs of beta cell proteins likely contribute to triggering beta cell destruction in Type 1 diabetes.
  • The immune response may target modified, not native, beta cell proteins.
  • The paradigm of Type 1 diabetes as a classical autoimmune disease warrants reconsideration.