Fructose consumption contributes to Hyperinsulinemia in adolescents with obesity through a GLP-1-mediated mechanism

In this 2019 double-blind crossover study, 14 lean adolescents and 23 adolescents with obesity underwent a baseline oral glucose tolerance test to determine their glucose tolerance and estimate insulin sensitivity and β-cell function [oral disposition index (oDIcpep)] and to confirm eligibility. Included participants were given 75g of either glucose or fructose as researchers collected their blood every 10 minutes for 60 minutes and measured their serum glucose, insulin, and GLP-1 (radioimmunoassay) and glucose-dependent insulinotropic polypeptide (GIP; ELISA). Galderisi et al. (2019) hypothesized that the GLP-1 and insulin response to glucose and fructose would vary between the lean and obese adolescents. Insulin and GLP-1 levels were higher in the obese adolescents than the lean participants following ingestion of fructose, although glucose responses and changes in GIP were not significantly different between the two groups. The GLP increment over the 60 minutes after fructose consumption was found to correlate with a lower oDIcpep (r2 = 0.22, P = 0.009). Whereas, GLP concentrations were higher in the lean subjects following the glucose challenge, relative to the obese individuals. Galderisi et al. (2019) concluded that fructose but not glucose elicits a greater GLP-1 and insulin response in adolescents with obesity than their leaner peers. It was suggested that fructose intake may be a factor, via a GLP-1-mediated mechanism, in the abnormally high levels of insulin seen in obese adolescents. [NPID: sugar, processed food, Western-style diet, soft drinks, glucose, fructose, insulin, obesity]

Year: 2019

Reference: Galderisi, A., Giannini, C., Van Name, M., & Caprio, S. (2019). Fructose consumption contributes to hyperinsulinemia in adolescents with obesity through a GLP-1-nediated mechanism. The Journal of clinical endocrinology and metabolism, 104(8), 3481–3490.