Elevations in blood glucose before and after the appearance of islet autoantibodies in children

Research output: Contribution to journalResearch articleContributedpeer-review

Contributors

  • Katharina Warncke - , Helmholtz Centre for Environmental Research, Technical University of Munich (Author)
  • Andreas Weiss - , Helmholtz Centre for Environmental Research (Author)
  • Peter Achenbach - , Helmholtz Centre for Environmental Research, Technical University of Munich (Author)
  • Thekla Von Dem Berge - , Children's Hospital Auf der Bult (Author)
  • Reinhard Berner - , Department of Paediatrics, University Hospital Carl Gustav Carus Dresden (Author)
  • Kristina Casteels - , KU Leuven (Author)
  • Lidia Groele - , Children's Clinical Hospital Józef Polikarp Brudzinski (Author)
  • Konstantinos Hatzikotoulas - , Helmholtz Centre for Environmental Research (Author)
  • Angela Hommel - , Center for Regenerative Therapies Dresden, Chair of Preclinical stem cell therapy and diabetes (Author)
  • Olga Kordonouri - , Children's Hospital Auf der Bult (Author)
  • Helena Elding Larsson - , Lund University (Author)
  • Markus Lundgren - , Lund University, Kristianstad Hospital (Author)
  • Benjamin A. Marcus - , Helmholtz Centre for Environmental Research, Technical University of Munich (Author)
  • Matthew D. Snape - , University of Oxford (Author)
  • Agnieszka Szypowska - , Medical University of Warsaw (Author)
  • John A. Todd - , University of Oxford (Author)
  • Ezio Bonifacio - , Center for Regenerative Therapies Dresden, Chair of Preclinical stem cell therapy and diabetes (Author)
  • Anette G. Ziegler - , Helmholtz Centre for Environmental Research, Technical University of Munich (Author)

Abstract

The etiology of type 1 diabetes has polygenic and environmental determinants that lead to autoimmune responses against pancreatic β cells and promote β cell death. The autoimmunity is considered silent without metabolic consequences until late preclinical stages,and it remains unknown how early in the disease process the pancreatic β cell is compromised. To address this, we investigated preprandial nonfasting and postprandial blood glucose concentrations and islet autoantibody development in 1,050 children with high genetic risk of type 1 diabetes. Pre-And postprandial blood glucose decreased between 4 and 18 months of age and gradually increased until the final measurements at 3.6 years of age. Determinants of blood glucose trajectories in the first year of life included sex, body mass index, glucose-related genetic risk scores, and the type 1 diabetes-susceptible INS gene. Children who developed islet autoantibodies had early elevations in blood glucose concentrations. A sharp and sustained rise in postprandial blood glucose was observed at around 2 months prior to autoantibody seroconversion, with further increases in postprandial and, subsequently, preprandial values after seroconversion. These findings show heterogeneity in blood glucose control in infancy and early childhood and suggest that islet autoimmunity is concurrent or subsequent to insults on the pancreatic islets.

Details

Original languageEnglish
Article numbere162123
JournalJournal of Clinical Investigation
Volume132
Issue number20
Publication statusPublished - 17 Oct 2022
Peer-reviewedYes

External IDs

PubMed 36250461

Keywords

Research priority areas of TU Dresden

Sustainable Development Goals

ASJC Scopus subject areas

Library keywords