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

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 t...

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Vydáno v:The Journal of clinical investigation Ročník 132; číslo 20; s. 1 - 10
Hlavní autoři: Warncke, Katharina, Weiss, Andreas, Achenbach, Peter, von dem Berge, Thekla, Berner, Reinhard, Casteels, Kristina, Groele, Lidia, Hatzikotoulas, Konstantinos, Hommel, Angela, Kordonouri, Olga, Elding Larsson, Helena, Lundgren, Markus, Marcus, Benjamin A., Snape, Matthew D., Szypowska, Agnieszka, Todd, John A., Bonifacio, Ezio, Ziegler, Anette-G.
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States American Society for Clinical Investigation 17.10.2022
Témata:
Age
Autoantibodies
Autoimmunity
Biomedical research
Blood Glucose
Blood sugar
Body mass index
Cell death
Child
Child, Preschool
Children
Clinical Medicine
Development and progression
Diabetes
Diabetes mellitus (insulin dependent)
Diabetes Mellitus, Type 1
Endocrinology and Diabetes
Endokrinologi och diabetes
Etiology
Genetic Predisposition to Disease
Genotype & phenotype
Glucose
Health aspects
Health risk assessment
Homeostasis
Humans
Immunology
INS gene
Insulin
Islands of Langerhans
Islets of Langerhans
Klinisk medicin
Measurement
Medical and Health Sciences
Medicin och hälsovetenskap
Metabolism
Pancreas
Pathogenesis
Pediatric research
Physiological aspects
Risk factors
Seroconversion
Type 1 diabetes
Germany
Insulin
Immunology
Diabetes
ISSN:1558-8238, 0021-9738, 1558-8238
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Shrnutí: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.
Bibliografie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
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ISSN:1558-8238
0021-9738
1558-8238
DOI:10.1172/JCI162123