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Population based study of prevalence of islet cell autoantibodies in monozygotic and dizygotic Danish twin pairs with insulin dependent diabetes mellitus

BMJ 1997; 314 doi: https://doi.org/10.1136/bmj.314.7094.1575 (Published 31 May 1997) Cite this as: BMJ 1997;314:1575
  1. Jacob S Petersen, scientista,
  2. Kirsten O Kyvik, assistant lecturerc,
  3. Polly J Bingley, professore,
  4. Edwin A M Gale, head of departmente,
  5. Anders Green, assistant lecturerc,
  6. Thomas Dyrberg, immunology managerb,
  7. Henning Beck-Nielsen, head of departmentd
  1. a Hagedorn Research Institute, DK-2820 Gentofte, Denmark
  2. b Novo Nordisk A/S, DK-2880 Bagsvaerd, Denmark
  3. c Genetic Epidemiology Research Unit, Institute of Community Health, Odense University, DK-5000 Odense, Denmark
  4. d Department of Endocrinology, Clinical Research Institute, Odense University Hospital, Odense
  5. e Diabetes and Metabolism, St Bartholomew's Hospital, London EC1A 7AB
  1. Correspondence and requests for reprints to: Dr J S Petersen ZymoGenetics, 1201 Eastlake Avenue East, Seattle, WA 98102, USA
  • Accepted 17 February 1997

Abstract

Objective: To study the comparative importance of environment and genes in the development of islet cell autoimmunity associated with insulin dependent diabetes mellitus.

Design: Population based study of diabetic twins.

Setting: Danish population.

Subjects: 18 monozygotic and 36 dizygotic twin pairs with one or both partners having insulin dependent diabetes.

Main outcome measures: Presence of islet cell antibodies, insulin autoantibodies, and autoantibodies to glutamic acid decarboxylase (GAD65) in serum samples from twin pairs 10 years (range 0-30 years) and 9.5 years (2-30 years) after onset of disease.

Results: In those with diabetes the prevalence of islet cell antibodies, insulin autoantibodies, and autoantibodies to glutamic acid decarboxylase in the 26 monozygotic twins was 38%, 85%, and 92%, respectively, and in the dizygotic twins was 57%, 70%, and 57%, respectively. In those without diabetes the proportions were 20%, 50%, and 40% in the 10 monozygotic twins and 26%, 49%, and 40% in the 35 dizygotic twins.

Conclusion: There is no difference between the prevalence of islet cell autoantibodies in dizygotic and monozygotic twins without diabetes, suggesting that islet cell autoimmunity is environmentally rather than genetically determined. Furthermore, the prevalence of islet cell antibodies was higher in the non-diabetic twins than in other first degree relatives of patients with insulin dependent diabetes. This implies that the prenatal or early postnatal period during which twins are exposed to the same environment, in contrast with that experienced by first degree relatives, is of aetiological importance.

Key messages

  • Autoantibodies against several islet cell antigens greatly increase the risk of developing insulin dependent diabetes

  • Development of islet cell autoimmunity is determined by enviromental rather than genetic factors

  • Fetal life is aetiologically important for induction of islet cell autoimmunity

  • Progression to clinical insulin dependent diabetes depends on genetically controlled responses to enviromental exposures after fetal life

Footnotes

  • Accepted 17 February 1997
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