1. GLP-1 receptor agonists are growth and differentiation factors for pancreatic islet beta cells.
- Author
-
Egan JM, Bulotta A, Hui H, and Perfetti R
- Subjects
- Animals, Cell Differentiation drug effects, Cell Differentiation physiology, Cell Division drug effects, Cell Division physiology, Glucagon physiology, Glucagon-Like Peptide 1, Glucagon-Like Peptide-1 Receptor, Growth Substances pharmacology, Growth Substances physiology, Humans, Islets of Langerhans drug effects, Peptide Fragments physiology, Protein Precursors physiology, Receptors, Glucagon physiology, Glucagon pharmacology, Islets of Langerhans cytology, Peptide Fragments pharmacology, Protein Precursors pharmacology, Receptors, Glucagon agonists
- Abstract
Glucagon-like peptide-1 (GLP-1) is an incretin hormone that, when given exogenously, is capable of normalizing blood glucose in individuals with type 2 diabetes. Until recently most of the research on this compound had been related to its insulinotropic properties. However, GLP-1 also regulates insulin synthesis and proinsulin gene expression, as well as the components of the glucose-sensing machinery. In addition to regulating insulin release, it is involved in regulating the secretion of at least two other islet hormones--glucagon and somatostatin. Extraislet effects of GLP-1 include a role in the central nervous system stress response, hypothalamic-pituitary function, and the suppression of gastric emptying. Recent studies from our own and other laboratories show that GLP-1 can regulate islet growth and is a differentiation factor of the endocrine pancreas. This leads us to propose that GLP-1 and GLP-1 receptor agonists, in the context of long-term treatment of type 2 diabetes, will have broader biological action on the endocrine pancreas than was earlier anticipated. We propose that GLP-1 is a growth factor for pancreatic endocrine cells and can increase islet cell mass. Here we review those reports that have highlighted its role as a factor for islet cell growth and differentiation., (Copyright 2003 John Wiley & Sons, Ltd.)
- Published
- 2003
- Full Text
- View/download PDF