Obesity and impairment of pancreatic beta-cellfunction in early adulthood, independent of obesity age of onset: The Santiago Longitudinal Study

Abstract

Aim: We investigated the relation of time of onset and length of obesity with biomarkers of beta-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-beta, 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-beta, 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 beta-cell functionality of NOBs, TOBs and FOBs.

Conclusions: Persistent and recent obesity are both related to IR, NAFL and a decline of beta-cell function in emerging adulthood. Defeating obesity in childhood or adolescence allows reaching emerging adulthood with beta-cell functioning similar to that of subjects who were NOB.