Aim
We investigated the relation of time of onset and length of obesity with biomarkers of β‐cell function in early adulthood in an infancy cohort.
Material and methods
In 1039 23‐year‐olds, body‐mass index (BMI) was measured at multiple time‐points from enrollment. BMI trajectories were interpolated with cubic polynomials. Fasting glucose, insulin and adiponectin were measured at 23 years. Homeostatic model assessment‐insulin resistance (HOMA‐IR), HOMA‐S, HOMA‐β, HOMA‐adiponectin (AD) and disposition index (DI) were estimated. IR and non‐alcoholic fatty liver (NAFL) were diagnosed. According to the BMI trajectory, five groups were defined: participants who were never obese (NOB); participants with obesity starting in adolescence and remained obese into adulthood (recent‐onset obesity, ROB); participants who were obese in early childhood but transitioned to non‐obesity as preadolescents (former obesity, FOB); participants who were obese in early childhood and remained obese into adulthood (persistent obesity, POB); participants with obesity starting in preadolescence and transitioned to non‐obesity as adolescents (transient obesity; TOB).
Results
Obesity was present in 47% of participants during at least one time‐point. ROBs and POBs had higher insulin, HOMA‐IR and HOMA‐β, lower HOMA‐S and DI, and higher prevalence of IR and NAFL at 23 years than NOBs, TOBs and FOBs. No differences were found in the β‐cell functionality of NOBs, TOBs and FOBs.
Conclusions
Persistent and recent obesity are both related to IR, NAFL and a decline of β‐cell function in emerging adulthood. Defeating obesity in childhood or adolescence allows reaching emerging adulthood with β‐cell functioning similar to that of subjects who were NOB.