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May 25, 2017Scientific ReportsOpen Access

GLP-1 receptor signalling promotes β-cell glucose metabolism via mTOR-dependent HIF-1α activation

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Authors

RCRodrigo CarlessiYCYounan ChenJRJordan Rowlands

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Overview

Laboratory study demonstrates enhanced glucose metabolism via mTOR and HIF-1α in pancreatic beta-cells, suggesting a gene-dependent pathway for chronic GLP-1-stimulated insulin secretion.

Key Points

  • To determine whether glucagon-like peptide-1 receptor signalling modulates glucose uptake and utilization in pancreatic β-cells.
  • Treated clonal BRIN-BD11 β-cells and rodent islets with 50 nM of the GLP-1 receptor agonist Exendin-4 for short durations and for 18 hours.
  • Assessed glucose uptake, consumption, glycolytic enzyme expression, ATP levels, and insulin secretion following Exendin-4 withdrawal.
  • Evaluated pathway dependency through HIF-1α gene depletion and pharmacological inhibition of PI3K or mTOR.
  • Prolonged 18-hour stimulation with Exendin-4 induced metabolic reprogramming, elevating glycolytic enzyme expression, glucose uptake, ATP levels, and post-washout insulin secretion.
  • HIF-1α depletion impaired the metabolic enhancements triggered by Exendin-4.
  • Pharmacological inhibition of either PI3K or mTOR completely abolished Exendin-4-driven increases in β-cell glucose metabolism.

Cite This Study

Carlessi et al. (2017) studied this question.

synapsesocial.com/papers/6a7dcdbe432a20ae7c150970https://doi.org/10.1038/s41598-017-02838-2
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