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Updated: Jan 26, 2026

Measuring Relative Insulin Secretion using a Co-Secreted Luciferase Surrogate
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Measuring Relative Insulin Secretion using a Co-Secreted Luciferase Surrogate

Published on: June 25, 2019

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CXCL14 Inhibits Insulin Secretion Independently of CXCR4 or CXCR7 Receptor Activation or cAMP Inhibition

Patricio Atanes1, Ross G Hawkes2, Oladapo E Olaniru2

  • 1Department of Diabetes, School of Life Course Sciences, Faculty of Life Sciences & Medicine, King's College London, London, UK, patricio.atanes_juiz@kcl.ac.uk.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|April 9, 2019
PubMed
Abstract

Insights

Chemokine CXCL14, found in islet delta-cells, inhibits insulin secretion by reducing beta-cell ATP levels. This suggests CXCL14 signaling inhibition could treat type 2 diabetes.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Metabolic Research

Background:

  • CXCL14 is a chemokine linked to obesity and insulin resistance.
  • Its role within pancreatic islets and beta-cells remains unclear.
  • Understanding CXCL14's function is crucial for metabolic disease research.

Purpose of the Study:

  • To investigate the function of CXCL14 in pancreatic beta-cells.
  • To determine the signaling pathways involved in CXCL14's effects.
  • To explore potential therapeutic targets for type 2 diabetes.

Main Methods:

  • Quantified Cxcl14 and Cxc-receptor mRNA using qPCR.
  • Determined CXCL14 localization in pancreatic islets via immunohistochemistry.
  • Assessed CXCL14 effects on insulin secretion, cAMP, glucose metabolism, and cell viability.

Main Results:

  • CXCL14 is localized to islet delta-cells in mice.
  • CXCL14 inhibited glucose-stimulated insulin secretion independently of CXCR4/CXCR7.
  • CXCL14 reduced beta-cell ATP production and glucose-6-phosphate generation.

Conclusions:

  • CXCL14, secreted by delta-cells, may paracrinely inhibit insulin secretion.
  • This inhibition occurs via reduced beta-cell ATP levels, independent of CXCR4/CXCR7.
  • Targeting CXCL14 signaling offers a potential strategy for treating type 2 diabetes.
Keywords:
CXCL14Insulin secretionIsletsMIN6 β-cellsType 2 diabetes

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