Obesity relates to the impairment of pancreatic β‐cell function in early adulthood, independent of age at obesity onset: Findings from the santiago longitudinal study

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 1,039 23-year-olds, BMI was measured at multiple time-points from enrollment. BMI trajectories were interpolated with cubic polynomials. Fasting glucose, insulin and adiponectin were measured at 23y. HOMA-IR, HOMA-S, HOMA-β, HOMA-AD and Disposition Index (DI) were estimated. Insulin resistance (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 23y 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, NAFLD 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 never obese. This article is protected by copyright. All rights reserved.