Incretin Hormones: Pathophysiological Risk Factors and Potential Targets for Type 2 Diabetes

Jared Rosenberg, Jordan Jacob, Priya Desai, Jeremy Park, Lorin Donovan, Joon Young Kim

Research output: Contribution to journalReview articlepeer-review

4 Scopus citations


Type 2 diabetes (T2D) is a multifaceted metabolic disorder associated with distinctive pathophysiological disturbances. One of the pathophysiological risk factors observed in T2D is a dysregulation of the incretin hormones glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 (GLP-1). Both hormones stimulate insulin secretion by acting postprandially on pancreatic β-cell receptors. Oral glucose administration stimulates increased insulin secretion in comparison with isoglycemic intravenous glucose administration, a phenomenon known as the incretin effect. While the evidence for incretin defects in individuals with T2D is growing, the etiology behind this attenuated incretin effect in T2D is not clearly understood. Given their central role in T2D pathophysiology, incretins are a promising target for T2D therapeutics. The present review synthesizes the recent attempts to explain the biological importance of incretin hormones and explore potential pharmacological approaches that target the incretins.

Original languageEnglish (US)
JournalJournal of obesity & metabolic syndrome
StateE-pub ahead of print - Sep 15 2021


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