Cantini Giulia, Di Franco Alessandra, Mannucci Edoardo, Luconi Michaela
Department of Experimental and Clinical Biomedical Sciences, Endocrinology Unit, University of Florence, Florence, Italy.
Department of Experimental and Clinical Biomedical Sciences, Endocrinology Unit, University of Florence, Florence, Italy; Diabetes Agency, Careggi Hospital, Florence, Italy.
Mol Cell Endocrinol. 2017 Jan 5;439:10-15. doi: 10.1016/j.mce.2016.10.013. Epub 2016 Oct 13.
Glucagon-like peptide 1(9-36) [GLP-1(9-36)] is generated by dipeptidyl peptidase-4 (DPP4) cleavage of the gut incretin hormone, GLP-1(7-36). Since GLP-1(9-36) has a very low affinity for the GLP-1 receptor (GLP-1R), it has so far been considered an inactive form of GLP-1. Here we show GLP-1(9-36) activity in human adipose stem cells (ASC) in vitro. GLP-1(9-36) inhibits human ASC proliferation, glucose uptake and adipogenesis, as well as induces cell apoptosis, to a similar extent as GLP-1(7-36) and liraglutide. Since GLP-1(9-36) effects are not reverted by the receptor antagonist exendin(9-39), which conversely reverts the effects of GLP-1(7-36), we hypothesized that the former may be mediated by a GLP-1 receptor different from the classical pancreatic one. This is the first report of GLP-1(9-36) activity in human adipose cells. Nevertheless, these findings deserve further preclinical studies to better elucidate novel and unforeseen GLP-1(9-36) activities, which could allow a better understanding of the clinical profile of DPP4 inhibitors and GLP-1R agonists.
