Fructose Consumption Contributes to Hyperinsulinemia in Adolescents With Obesity Through a GLP-1–Mediated Mechanism

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.

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Objective

• To
  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.

Background

• 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.

Methods

• Fourteen
  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. 
• Participants
  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.
• Plasma
  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.

Findings

• 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
  both groups.
• 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.

Conclusions

• Fructose,
  but not glucose, ingestion elicits a higher GLP-1 and insulin response in
  adolescents with obesity than in lean adolescents.
• Fructose
  consumption may contribute to the hyperinsulinemic phenotype of adolescent
  obesity through a GLP-1–mediated mechanism.

Points
to Consider:

• Given the small size and age of the sample, the
  generalizability of these results is limited.

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