1318-P: Fructose Consumption Contributes to Hyperinsulinemia in Obese Adolescents through a GLP-1-Mediated Mechanism

Abstract

Background: The consumption of high-fructose beverages is associated with higher risk for T2D. Fructose can stimulate GLP-1 secretion in lean adults, in the absence of any inhibitory effect on appetite. We hypothesized that the ingestion of glucose (GLC) and fructose (FRU) may differentially stimulate GLP-1 and insulin response in lean and obese adolescents. Methods: We studied 14 lean (4F, 15.9±1.6y, 21.8±2.2 kg/m2) and 23 obese (5F, 15.1±1.6y, 34.5±4.6 kg/m2) adolescents. Participants received, in a double blinded cross-over study, 75g of GLC or FRU. Plasma was obtained every 10min for 60 minutes GLC was determined by YSI Analyzer; insulin and GLP-1 were measured by Millipore RIA; data were expressed as incremental values from baseline and compared by linear mixed effect model between lean and obese. Results: Obese adolescents exhibited greater insulin (p<0.001) and GLP-1 (p<0.001) rise after FRU than lean peers, at each time points (Figure), in the absence of a significant difference in plasma GLC (p0.699). After GLC ingestion, neither the rise in plasma GLC (p0.099), nor in insulin (p0.099) and GLP-1(p0.083) differed between lean and obese youths. Conclusion: Fructose, but not glucose, ingestion elicits higher insulin and GLP-1 response in obese as compared to lean adolescents. High-fructose consumption may contribute to the hyperinsulinemic phenotype through a GLP-1 mediated mechanism. Disclosure A. Galderisi: None. M.A. Van Name: Research Support; Self; Novo Nordisk Inc. C. Giannini: None. M. Savoye: None. S. Caprio: None. Funding National Institutes of Health (1R01DK085577-01, R01HD40787, R01HD28016; P30DK045735, K12DK094714-02; R01DK111038-01A1; Pediatric Endocrine Society; Robert E. Leet and Clara Guthrie Patterson Trust; European Medical International Framework (EMIF115372)