J Clin Endocrinol Metab. 2019 Aug 1;104(8):3481-3490. doi: 10.1210/jc.2019-00161
Galderisi A, Giannini C, van Name M, et al.
test the hypothesis that that the ingestion of glucose and fructose may
differentially stimulate GLP-1 and insulin response in lean adolescents
and adolescents with obesity.
- The consumption of high-fructose beverages is
associated with a higher risk for obesity and diabetes.
- Fructose can stimulate glucagon-like peptide 1
(GLP-1) secretion in lean adults, in the absence of any anorexic effect.
- It is unclear whether the same or similar
effect occurs in lean and obese adolescents.
lean adolescents and twenty-three obese adolescents were included in the
study. The average BMI was approximately 22 in the lean group and
approximately 35 in the obese group.
The average age in both groups was approximately 16.
underwent a baseline oral glucose tolerance test to determine their
glucose tolerance and estimate insulin sensitivity and β-cell function [oral
disposition index (oDIcpep)]. In a double-blind, crossover design, eligible
subjects received 75 g of glucose or fructose.
was obtained every 10 minutes for 60 minutes for the measures of glucose,
insulin, and GLP-1 (radioimmunoassay) and glucose-dependent insulinotropic
polypeptide (GIP; ELISA). Incremental glucose and hormone levels were
compared between lean individuals and those with obesity by a linear mixed
model. The relationship between GLP-1 increment and oDIcpep was evaluated
by regression analysis.
- Following the fructose challenge, plasma
glucose excursions were similar in both groups, yet the adolescents in the
obese group exhibited a greater insulin (P < 0.001) and GLP-1 (P <
0.001) increase than did their lean peers. Changes in GIP were similar in
- After glucose ingestion, the GLP-1 response (P
< 0.001) was higher in the lean group. The GLP-1 increment during 60
minutes from fructose drink was correlated with a lower oDIcpep.
but not glucose, ingestion elicits a higher GLP-1 and insulin response in
adolescents with obesity than in lean adolescents.
consumption may contribute to the hyperinsulinemic phenotype of adolescent
obesity through a GLP-1–mediated mechanism.
- Given the small size and age of the sample, the
generalizability of these results is limited.