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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 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.
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
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...
Insulin: Dosing Regimen and Adverse Effects01:16

Insulin: Dosing Regimen and Adverse Effects

Insulin-replacement therapy usually includes both long-acting insulin (basal) and short-acting insulin (to cater to postprandial needs). In a diverse group of type 1 diabetes patients, the average daily insulin dose is typically 0.5-0.7 units/kg body weight. However, obese patients and pubertal adolescents may need more due to insulin resistance.
The basal dose constitutes about 40%-50% of the total daily dose, with the rest as premeal insulin. The mealtime insulin dose should mirror...
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...

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Related Experiment Video

Updated: Jun 24, 2026

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
09:48

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance

Published on: February 17, 2023

Type B insulin resistance developing during interferon-alpha therapy.

Amanda L Daniel1, Josetta L Houlihan, Janice S Blum

  • 1Division of Endocrinology and Metabolism, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Endocrine Practice : Official Journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
|March 18, 2009
PubMed
Summary
This summary is machine-generated.

A rare case of diabetes, type B insulin resistance, developed in a patient treated for hepatitis C with interferon-alpha and ribavirin. Insulin receptor autoantibodies emerged during therapy, resolving after its discontinuation.

Related Experiment Videos

Last Updated: Jun 24, 2026

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
09:48

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance

Published on: February 17, 2023

Area of Science:

  • Endocrinology
  • Hepatology
  • Immunology

Background:

  • Hepatitis C is often treated with interferon-alpha and ribavirin.
  • Type B insulin resistance is a rare condition characterized by autoantibodies against the insulin receptor.
  • Interferon therapy can induce autoimmune phenomena.

Observation:

  • A 55-year-old man with hepatitis C developed severe hyperglycemia and insulin resistance during interferon-alpha and ribavirin treatment.
  • The patient presented with rapid onset hyperglycemia, profound weakness, and weight loss.
  • High insulin infusion rates were required to manage hyperglycemia.

Findings:

  • Insulin receptor autoantibodies were detected in the patient's serum.
  • Discontinuation of interferon-alpha and ribavirin led to a spontaneous decline in insulin requirements.
  • Insulin receptor autoantibodies were no longer detectable after 6 months, and the patient became euglycemic.

Implications:

  • This case highlights a rare complication of interferon-alpha therapy: type B insulin resistance due to autoantibodies.
  • It suggests a potential link between interferon-induced autoimmunity and the development of insulin resistance.
  • Physicians should consider monitoring for autoimmune complications in patients receiving interferon-based therapies.