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

Amelia Linnemann, Dawn Belt Davis

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)44-49
Number of pages6
JournalJournal of Diabetes Investigation
Volume7
DOIs
StatePublished - Apr 1 2016
Externally publishedYes

Fingerprint

Glucagon-Like Peptide 1
Cholecystokinin
Islets of Langerhans
Incretins
Obesity
Paracrine Communication
Blood Glucose
Cell Survival
Hormones
Insulin
Therapeutics

Keywords

  • Cholecystokinin
  • Glucagon-like peptide-1
  • Pancreatic islet

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

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