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Related Concept Videos

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 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...
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...
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 I Diabetes III: Clinical Manifestations01:19

Type I Diabetes III: Clinical Manifestations

Type 1 diabetes mellitus typically presents with rapid-onset symptoms due to the body’s inability to utilize glucose in the absence of insulin. Since insulin is required for glucose uptake into cells, its deficiency leads to hyperglycemia and cellular energy deprivation, resulting in characteristic clinical features.Polyuria and PolydipsiaOne of the earliest, most prominent symptoms is polyuria (excessive urination). When blood glucose concentrations rise above the renal threshold, the kidneys...
Pathophysiology of Diabetes01:20

Pathophysiology of Diabetes

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, suggesting a...

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

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The case for virus-induced type 1 diabetes.

Isabella Spagnuolo1, Aurora Patti, Guido Sebastiani

  • 1Diabetes Unit, Department of Medicine, Surgery and Neuroscience, University of Siena, Toscana Life Science Park, Siena, Italy.

Current Opinion in Endocrinology, Diabetes, and Obesity
|June 8, 2013
PubMed
Summary

Viral infections may contribute to type 1 diabetes (T1D) by damaging pancreatic beta-cells and triggering inflammation. This suggests that antiviral strategies could be key in protecting these vital cells.

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Area of Science:

  • Immunology
  • Virology
  • Endocrinology

Background:

  • Type 1 diabetes (T1D) arises from immune-mediated destruction of pancreatic beta-cells, influenced by genetic, immune, and environmental factors.
  • A potential role for viral infections in T1D pathogenesis has been long hypothesized, with recent molecular and cellular studies providing new insights.

Purpose of the Study:

  • To review the evidence linking viral infections to the pathogenesis of type 1 diabetes.
  • To explore the mechanisms by which viruses may contribute to beta-cell damage and inflammation in the pancreas.

Main Methods:

  • Review of recent studies on viral infections and T1D.
  • Analysis of molecular and cellular data from animal models and human pancreatic tissue.
  • Investigation of immune responses, including innate immunity, in T1D pathogenesis.

Main Results:

  • Studies confirm that viruses can infect pancreatic beta-cells, leading to islet inflammation and impaired function.
  • In-situ investigations reveal that both adaptive and innate immune responses are involved in T1D.
  • Immune-mediated phenomena infiltrate the entire pancreas, not just the endocrine portion.

Conclusions:

  • Inflammation is integral to the insulitic process in T1D.
  • Growing evidence supports the contribution of viral infections to a proinflammatory pancreatic environment.
  • Viruses may play a role in beta-cell damage and dysfunction, supporting the development of antiviral therapies for T1D prevention.