Glucagon-like peptide-1 and cholecystokinin production and signaling in the pancreatic islet as an adaptive response to obesity

J Diabetes Investig. 2016 Apr;7 Suppl 1(Suppl 1):44-9. doi: 10.1111/jdi.12465. Epub 2016 Mar 14.


Precise control of blood glucose is dependent on adequate β-cell mass and function. Thus, reductions in β-cell mass and function lead to insufficient insulin production to meet demand, and result in diabetes. Recent evidence suggests that paracrine signaling in the islet might be important in obesity, and disruption of this signaling could play a role in the pathogenesis of diabetes. For example, we recently discovered a novel islet incretin axis where glucagon-like peptide-1 regulates β-cell production of another classic gut hormone, cholecystokinin. This axis is stimulated by obesity, and plays a role in enhancing β-cell survival. In the present review, we place our observations in the wider context of the literature on incretin regulation in the islet, and discuss the potential for therapeutic targeting of these pathways.

Keywords: Cholecystokinin; Glucagon‐like peptide‐1; Pancreatic islet.

Publication types

  • Review

MeSH terms

  • Animals
  • Cholecystokinin / biosynthesis*
  • Cholecystokinin / metabolism*
  • Glucagon-Like Peptide 1 / metabolism*
  • Humans
  • Incretins / metabolism
  • Islets of Langerhans / metabolism*
  • Obesity / metabolism*
  • Paracrine Communication*


  • Incretins
  • Glucagon-Like Peptide 1
  • Cholecystokinin