PuSH - Publikationsserver des Helmholtz Zentrums München

Warncke, K. ; Weiss, A. ; Achenbach, P. ; von dem Berge, T.* ; Berner, R.* ; Casteels, K.* ; Groele, L.* ; Hatzikotoulas, K. ; Hommel, A. ; Kordonouri, O.* ; Elding Larsson, H.* ; Lundgren, M.* ; Marcus, B.A. ; Snape, M.D.* ; Szypowska, A.* ; Todd, J.A.* ; Bonifacio, E. ; Ziegler, A.-G.

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

J. Clin. Invest. 132:e162123 (2022)
Verlagsversion Forschungsdaten DOI
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
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.
Altmetric
Weitere Metriken?
Zusatzinfos bearbeiten [➜Einloggen]
Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Diabetes ; Immunology ; Insulin
ISSN (print) / ISBN 0021-9738
e-ISSN 1558-8238
Quellenangaben Band: 132, Heft: 20, Seiten: , Artikelnummer: e162123 Supplement: ,
Verlag American Society of Clinical Investigation
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes Research Type 1 (IDF)
Institute of Translational Genomics (ITG)
Institute for Pancreatic Beta Cell Research (IPI)