| Original language | English |
|---|---|
| Title of host publication | Diapedia : The living textbook of diabetes |
| Number of pages | 3 |
| Publisher | European Association for the Study of Diabetes (EASD) |
| Publication date | 12 Jun 2014 |
| Pages | 1-3 |
| Chapter | Metabolism, Incretins, Incretin physiology and its history, Incretin secretion: direct mechanisms |
| DOIs | |
| Publication status | Published - 12 Jun 2014 |
Abstract
The incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are secreted from gastro-intestinal K- and L-cells, respectively, and play an important role in post-prandial blood glucose regulation. They do this by direct stimulation of the pancreatic β-cell, accounting for some 25-70% of postprandial insulin secretion in healthy subjects. In patients with type 2 diabetes (T2D, however, this effect is greatly reduced or lost due to a combination of severely impaired or eliminated insulinotrophic effect of GIP and reduced meal stimulated GLP-1 secretion. This suggests that the therapeutic potential of GIP for the treatment for T2D is limited, whereas GLP-1 based treatments have been on the market since 2005. Research is now pursuing novel approaches to utilize the effects of GLP-1 for T2D treatment. A combinatorial approach by which the activity of the major enzyme responsible for incretin degradation (dipeptidyl peptidase-4) is inhibited (drugs are already on the market) while the secretion of endogenous GLP-1 secretion is stimulated at the same time may prove particularly rewarding. In this section we review current knowledge on the mechanisms for direct activation of GIP and GLP-1 secretion.
Keywords
- Faculty of Health and Medical Sciences
- GIP
- GLP-1
- Direct mechanisms of secretion
