In children, the mechanisms implicated in deterioration of
glucose homeostasis versus reversion to normal
glucose tolerance (NGT) remain uncertain. We aimed to describe the natural history of dysglycemia from childhood to late adolescence and to identify its early determinants. We used baseline (8-10 years, n = 630), 1st follow-up (10-12 years, n = 564) and 2nd follow-up (15-17 years, n = 377) data from the QUALITY cohort of White Canadian children with parental
obesity. Children underwent a 2-h oral
glucose tolerance test at each cycle with plasma
glucose and
insulin measured at 0/30/60/90/120 min. American Diabetes Association criteria defined dysglycemia (impaired fasting
glucose,
impaired glucose tolerance or
type 2 diabetes). Longitudinal patterns of
insulin sensitivity and beta-cell function were estimated using generalized additive mixed models. Model averaging identified biological, sociodemographic and lifestyle-related determinants of dysglycemia. Of the children NGT at baseline, 66 (21%) developed dysglycemia without reverting to NGT. Among children with dysglycemia at baseline, 24 (73%) reverted to NGT. In children with dysglycemia at 1st follow-up, 18 (53%) later reverted to NGT. Among biological, sociodemographic and lifestyle determinants at 8-10 years, only fasting and 2-h
glucose were associated with developing dysglycemia (odds ratio [95% CI] per 1 mmol/L increase: 4.50 [1.06; 19.02] and 1.74 [1.11; 2.73], respectively). Beta-cell function decreased by 40% in children with
overweight or
obesity. In conclusion, up to 75% of children with dysglycemia reverted to NGT during puberty. Children with higher fasting and 2-h
glucose were at higher risk for progression to dysglycemia, while no demographic/lifestyle determinants were identified.