Article Text

PDF
Mitochondrial DNA haplogroups and type 2 diabetes: a study of 897 cases and 1010 controls
  1. P F Chinnery1,
  2. C Mowbray1,
  3. S K Patel2,
  4. J L Elson1,
  5. M Sampson3,
  6. G A Hitman4,
  7. M I McCarthy5,
  8. A T Hattersley6,
  9. M Walker2
  1. 1Mitochondrial Research Group, Newcastle University, Newcastle upon Tyne, UK
  2. 2Diabetes Research Group, Newcastle University, Newcastle upon Tyne, UK
  3. 3Department of Diabetes and Endocrinology, Norfolk and Norwich University Hospital NHS Trust, Norwich, UK
  4. 4Centre for Diabetes and Metabolic Medicine, Bart’s and The London Queen Mary’s School of Medicine and Dentistry, London, UK
  5. 5Oxford Centre for Diabetes, Endocrinology and Metabolism, Oxford, UK
  6. 6Centre for Molecular Genetics, Peninsula Medical School, Exeter, UK
  1. Correspondence to:
 Professor P F Chinnery
 Mitochondrial Research Group, The Medical School, Framlington Place, Newcastle upon Tyne NE2 4HH, UK; p.f.chinnery{at}ncl.ac.uk

Abstract

Mitochondria play a central role in the secretion of insulin by pancreatic β-cells, and pathogenic mutations of mitochondrial DNA (mtDNA) can cause diabetes. The aetiology of type 2 diabetes has a strong genetic component, raising the possibility that genetic variants of mtDNA alter the risk of developing the disorder. Recent studies have produced conflicting results. By studying 897 UK cases of type 2 diabetes and 1010 population-matched controls, it is shown that European mtDNA haplogroups are unlikely to play a major role in the risk of developing the disorder.

  • OXPHOS, oxidative phosphorylation
  • mtDNA, mitochondrial DNA

Statistics from Altmetric.com

Footnotes

  • Competing interests: None declared.

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.