Related Experiment Video

Updated: May 27, 2026

Generation of High Quality Chromatin Immunoprecipitation DNA Template for High-throughput Sequencing (ChIP-seq)
09:52

Generation of High Quality Chromatin Immunoprecipitation DNA Template for High-throughput Sequencing (ChIP-seq)

Published on: April 19, 2013

Cesarean section and interferon-induced helicase gene polymorphisms combine to increase childhood type 1 diabetes

Ezio Bonifacio1, Katharina Warncke, Christiane Winkler

  • 1Center for Regenerative Therapies, Dresden University of Technology, Dresden, Germany.

Diabetes
|November 24, 2011
PubMed

Insights

Cesarean delivery increases type 1 diabetes risk in children, particularly those with specific IFIH1 gene variants. This risk appears linked to viral responses during the preclinical autoimmune phase.

Area of Science:

  • Immunology
  • Endocrinology
  • Genetics

Background:

  • Type 1 diabetes incidence is rising globally.
  • Cesarean delivery rates are also increasing.
  • A potential link between cesarean delivery and type 1 diabetes risk is suggested.

Purpose of the Study:

  • To investigate the association between cesarean delivery and the risk of islet autoimmunity and type 1 diabetes.
  • To examine the role of genes involved in type 1 diabetes susceptibility in this association.

Main Methods:

  • A cohort of 1,650 children born to parents with type 1 diabetes was followed from birth.
  • Cesarean section was analyzed as a risk factor for developing islet autoantibodies and type 1 diabetes.
  • Genetic analysis included HLA genotypes and immune response genes like IFIH1.

Main Results:

  • Children born via cesarean section had over twofold higher risk for type 1 diabetes (HR 2.5).
  • Cesarean delivery accelerated progression to diabetes post-autoimmunity but did not increase autoimmunity risk.
  • An interaction was observed between cesarean delivery and IFIH1 genotypes, significantly increasing type 1 diabetes risk.

Conclusions:

  • Cesarean delivery may modify type 1 diabetes risk, potentially through effects on viral responses.
  • The findings highlight a gene-environment interaction involving cesarean delivery and IFIH1 in type 1 diabetes development.
Abstract

More Related Videos

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells06:27

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

Published on: May 6, 2013

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes10:00

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes

Published on: March 24, 2015

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...
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: 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...
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...
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...