title: Association between impaired fasting glycaemia in pediatric obesity and type 2 diabetes in young adulthood.
abstract: In adults, impaired fasting glycemia (IFG) increases the risk for type 2 diabetes mellitus (T2DM). This study aimed to investigate to which extent children with obesity develop T2DM during early adulthood, and to determine whether IFG and elevated hemoglobin A1c (HbA1c) in obese children are risk markers for early development of T2DM.
  
  
  
  In this prospective cohort study, 1620 subjects from the Swedish Childhood Obesity Treatment Registry - BORIS who were ⩾18 years at follow-up and 8046 individuals in a population-based comparison group, matched on gender age and living area, were included. IFG was defined according to both ADA (cut-off 5.6 mmol l(-1)) and WHO (6.1 mmol l(-1)). Elevated HbA1c was defined according to ADA (cut-off 39 mmol l(-1)). Main outcome was T2DM medication, as a proxy for T2DM. Data on medications were retrieved from a national registry.
  
  
  
  The childhood obesity cohort were 24 times more likely to receive T2DM medications in early adulthood compared with the comparison group (95% confidence interval (CI): 12.52-46). WHO-defined IFG predicted future use of T2DM medication with an adjusted hazard ratio (HR) of 3.73 (95% CI: 1.87-7.45) compared with those who had fasting glucose levels <5.6 mmol l(-1). A fasting glucose level of 5.6-6.0 mmol l(-1), that is, the IFG-interval added by American Diabetes Association (ADA), did not increase the use of T2DM medication more than pediatric obesity itself, adjusted HR=1.72 (0.84-3.52). Elevated levels of HbA1c resulted in an adjusted HR=3.12 (1.50-6.52). More severe degree of obesity also increased the future T2DM risk.
  
  
  
  IFG according to WHO and elevated HbA1c (39-48 mmol l(-1)), but not the additional fasting glucose interval added by ADA (5.6-6.0 mmol l(-1)), can be considered as prediabetes in the obese pediatric population in Sweden.
authors.affiliation: Division of Pediatrics, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.
authors.forename: E
authors.identifier: 0000-0003-1433-2295
authors.initials: E
authors.lastname: Hagman
authors.affiliation: Division of Pediatrics, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.
authors.forename: P
authors.initials: P
authors.lastname: Danielsson
authors.affiliation: Unit of Clinical Epidemiology, Department of Medicine/Solna, Karolinska Institutet, Stockholm, Sweden.
authors.forename: L
authors.initials: L
authors.lastname: Brandt
authors.affiliation: Unit of Clinical Epidemiology, Department of Medicine/Solna, Karolinska Institutet, Stockholm, Sweden.
authors.forename: A
authors.initials: A
authors.lastname: Ekbom
authors.affiliation: Division of Pediatrics, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.
authors.forename: C
authors.initials: C
authors.lastname: Marcus
mesh_terms: D000293:Adolescent; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D002648:Child; D003924:Diabetes Mellitus, Type 2 / Q000097:blood*; D005215:Fasting / Q000097:blood*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D063766:Pediatric Obesity / Q000097:blood*; D011236:Prediabetic State / Q000097:blood; D011446:Prospective Studies; D012042:Registries; D013548:Sweden; D055815:Young Adult
chemical_list: D001786:Blood Glucose