<b>NEW & NOTEWORTHY</b> Therapeutic activation of endogenous glucagon-like peptide 2 (GLP-2) secretion is a promising strategy to improve intestinal adaptation in patients with short bowel syndrome.
With the introduction of glucagon-like peptide-2 (GLP-2) in the treatment of short bowel syndrome (SBS), there is emerging evidence that GLP-2 may play a role in the restoration of the disturbed homeostatic feedback in the gut-liver axis and may ameliorate SBS-associated liver damage.
Teduglutide is an analog of glucagon-like peptide 2 (GLP-2) which is approved for the treatment of patients with short bowel syndrome (SBS) who are dependent on parenteral support.
The discovery that GLP-2 promotes mucosal growth in the intestine is described, and key findings from both preclinical studies and the GLP-2 clinical development program for short bowel syndrome (SBS) are reviewed.
Glucagon-like peptide-2 (GLP-2) affects multiple facets of gastrointestinal physiology and have been used to treat patients with short bowel syndrome, but the distribution of its receptor (GLP2R) in human remains poorly understood.
To determine whether these growth factors exert synergistic effects on intestinal growth and function, GLP-2 and EGF-containing media (EGF-cm) were administered, alone and in combination, in neonatal piglet models of short bowel syndrome (SBS).
GLP-2, despite its known trophic and anti-inflammatory intestinal actions translated into preliminary clinical studies using the GLP-2 analogue teduglutide for treatment of short bowel syndrome and Crohn's disease, remains poorly characterized in terms of expression of its receptor in tissues of interest.
In this review, the nature of short-bowel syndrome is described and the antisecretory, transit modulating and intestinotrophic effects of GLP-2 are presented.