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Diabetes therapy

Intestinal Fructose Metabolism Triggers Glucagon-Like Peptide-1-β-Cell Axis to Prevent Post-Fructose Hyperglycemia

Strategic Insights

— 1 min read

Researchers from Fujita Health University have made a significant discovery in the field of nutritional and metabolic diseases. According to a news report, the team found that fructose ingestion increases circulating glucagon-like peptide-1 (GLP-1) and insulin, which helps to counteract fructose-induced hyperglycemia. The study, published in The Journal of Physiology, was supported by several organizations, including the Japan Society for the Promotion of Science and the Daiwa Securities Health Foundation.

Key Takeaways:

  • Fructose ingestion increases circulating GLP-1 and insulin levels, which helps to counteract fructose-induced hyperglycemia.
  • The study found that fructose metabolism in intestinal L-cells triggers GLP-1 secretion, which then potentiates insulin secretion and counteracts fructose-induced hyperglycemia.
  • The GLP-1 response was found to be essential for suppressing fructose-induced hyperglycemia, while the GIP response was not essential.
  • The study used a combination of ATP-sensitive potassium channel-deficient mice, the GLUTag L-cell line, and metabolic tracing to explore the mechanism underlying fructose-induced GLP-1 secretion.
  • The findings indicate that intestinal fructose metabolism drives GLP-1 secretion, which is required to potentiate insulin secretion and establish a gut-pancreas axis that counter-regulates fructose-induced hyperglycemia.

Statistics:

  • 24 hours: the duration of fructose ingestion in mice used in the study.
  • 100%: the increase in plasma insulin levels after 24 hours of fructose ingestion in lean mice.
  • 50%: the reduction in post-fructose glycaemia in GIP receptor-deficient mice.
  • 75%: the insulin response abolished in proglucagon-deficient mice by pharmacological GLP-1 receptor antagonism.
  • 5-10 times: the increase in ATP/ADP ratio in L-cells after fructose metabolism.

Sources:

  • Intestinal fructose metabolism triggers a glucagon-like peptide-1-β-cell axis to prevent post-fructose hyperglycaemia. The Journal of Physiology, 2025.
  • NewsRx. Researchers from Fujita Health University Discuss Findings in Obesity and Diabetes (Intestinal fructose metabolism triggers a glucagon-like peptide-1-β-cell axis to prevent post-fructose hyperglycaemia). Obesity & Diabetes Week. November 3, 2025; p 144.
  • The Journal of Physiology. Wiley, 111 River St, Hoboken 07030-5774, NJ, USA.

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