ESPE Abstracts

Background: Asprosin is an adipokine involved in glucose homeostasis and its plasma levels physiologically increases in fasting conditions and decreases with refeeding. In non-diabetic children and adolescents with obesity, insulin resistance (IR) and impaired fasting glucose (IFG) seem to influence the physiological variation in meal-related asprosin levels 120 minutes after an oral glucose load (Corica et al. doi:10.3389/fendo.2021.805700). No data are available on plasma asprosin levels at 60 minutes after a meal in children and adolescents with obesity.

Objectives: To evaluate the dynamics of asprosin secretion at fasting and 60 and 120 minutes after meal intake, with particular interest in the trend of asprosin levels at 60 minutes with respect to fasting and 120 minutes levels

Methods: Seventy-nine obese subjects were recruited (aged 11.5 ± 2.6 years). Children underwent clinical and biochemical assessments, including oral glucose tolerance test (OGTT). Monophasic or biphasic blood glucose shape trends were assessed. IR was defined as HOMA-IR > 2.5 in prepubertal children and > 4 in pubertal subjects. IFG was defined as fasting plasma glucose between 100 and 125 mg/dL. Asprosin serum levels were measured by an ELISA at fasting and at 60-minute and 120-minute OGTT timepoints. Applying Mc Wolfe's non-parametric test, trends in asprosin levels among fasting, 60-minute and 120-minute OGTT timepoints were assessed in the entire study population as well as in subgroups divided according to the presence of IR, IFG and glucose shape trend.

Results: A significant change in asprosin levels between 0, 60 and 120 minutes was demonstrated in the entire study population. Specifically, evaluation of meal-related asprosin dynamics documented that the increase between fasting and 60-minute levels and the decrease between 60-minute and 120-minute levels were significant (P=0.004). The same trend in asprosin levels was also documented among subjects with IFG (P=0.024), IR (P=0.037), and those with a monophasic glucose shape pattern (P=0.021). The variation of asprosin levels was not significant among non-IFG and non-IR patients and among those with a biphasic glucose curve pattern.

Conclusions: The analysis of the dynamic of asprosin levels carried out on three assessments in obese children with IFG and/or IR and/or a monophasic glucose shape pattern, supporting the hypothesis of a potential impairment of meal-related asprosin levels in these subjects. These results suggest that an altered asprosin secretion might be an early biomarker of impaired glucose regulation and IR.