Tags

Type your tag names separated by a space and hit enter

The environment and the origins of islet autoimmunity and Type 1 diabetes.
Diabet Med 2013; 30(2):155-60DM

Abstract

Type 1 diabetes involves the specific destruction of the pancreatic islet β-cells, eventually resulting in a complete dependency of exogenous insulin. The clinical onset of diabetes is preceded by the appearance of autoantibodies against β-cell antigens. The human leukocyte antigen (HLA) region is the single most important genetic determinant of Type 1 diabetes susceptibility, yet variability in the HLA region has been estimated to explain only approximately 60% of the genetic influence of the disease. Over 50 identified non-HLA genetic polymorphisms support the notion that genetics alone cannot explain Type 1 diabetes. Several lines of evidence indicate that environmental triggers may be integral in inducing the onset of islet autoimmunity in genetically susceptible individuals. The association between environmental factors and the clinical onset is complicated by observation that the rate of progression to clinical onset may be affected by environmental determinants. Hence, the environment may be aetiological as well as pathogenic. Putative inductive mechanisms include viral, microbial, diet-related, anthropometric and psychosocial factors. Ongoing observational cohort studies such as The Environmental Determinants of Diabetes in the Young (TEDDY) study aim to ascertain environmental determinants that may trigger islet autoimmunity and either speed up or slow down the progression to clinical onset in subjects with persistent islet autoimmunity.

Authors+Show Affiliations

Department of Clinical Sciences, Lund University/CRC, Skåne University Hospital SUS, Malmö, Sweden.No affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

23252770

Citation

Eringsmark Regnéll, S, and A Lernmark. "The Environment and the Origins of Islet Autoimmunity and Type 1 Diabetes." Diabetic Medicine : a Journal of the British Diabetic Association, vol. 30, no. 2, 2013, pp. 155-60.
Eringsmark Regnéll S, Lernmark A. The environment and the origins of islet autoimmunity and Type 1 diabetes. Diabet Med. 2013;30(2):155-60.
Eringsmark Regnéll, S., & Lernmark, A. (2013). The environment and the origins of islet autoimmunity and Type 1 diabetes. Diabetic Medicine : a Journal of the British Diabetic Association, 30(2), pp. 155-60. doi:10.1111/dme.12099.
Eringsmark Regnéll S, Lernmark A. The Environment and the Origins of Islet Autoimmunity and Type 1 Diabetes. Diabet Med. 2013;30(2):155-60. PubMed PMID: 23252770.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The environment and the origins of islet autoimmunity and Type 1 diabetes. AU - Eringsmark Regnéll,S, AU - Lernmark,A, PY - 2012/11/12/received PY - 2012/11/29/revised PY - 2012/12/06/accepted PY - 2012/12/21/entrez PY - 2012/12/21/pubmed PY - 2013/7/31/medline SP - 155 EP - 60 JF - Diabetic medicine : a journal of the British Diabetic Association JO - Diabet. Med. VL - 30 IS - 2 N2 - Type 1 diabetes involves the specific destruction of the pancreatic islet β-cells, eventually resulting in a complete dependency of exogenous insulin. The clinical onset of diabetes is preceded by the appearance of autoantibodies against β-cell antigens. The human leukocyte antigen (HLA) region is the single most important genetic determinant of Type 1 diabetes susceptibility, yet variability in the HLA region has been estimated to explain only approximately 60% of the genetic influence of the disease. Over 50 identified non-HLA genetic polymorphisms support the notion that genetics alone cannot explain Type 1 diabetes. Several lines of evidence indicate that environmental triggers may be integral in inducing the onset of islet autoimmunity in genetically susceptible individuals. The association between environmental factors and the clinical onset is complicated by observation that the rate of progression to clinical onset may be affected by environmental determinants. Hence, the environment may be aetiological as well as pathogenic. Putative inductive mechanisms include viral, microbial, diet-related, anthropometric and psychosocial factors. Ongoing observational cohort studies such as The Environmental Determinants of Diabetes in the Young (TEDDY) study aim to ascertain environmental determinants that may trigger islet autoimmunity and either speed up or slow down the progression to clinical onset in subjects with persistent islet autoimmunity. SN - 1464-5491 UR - https://www.unboundmedicine.com/medline/citation/23252770/The_environment_and_the_origins_of_islet_autoimmunity_and_Type 1_diabetes_ L2 - https://doi.org/10.1111/dme.12099 DB - PRIME DP - Unbound Medicine ER -