GLP1 and cancer: friend or foe?
- 1Laboratory of Experimental Medicine and Endocrinology, Catholic University of Leuven, Leuven, Belgium
2Departments of Internal Medicine
3Endocrinology, University Hospitals Leuven, Leuven, Belgium
- (Correspondence should be addressed to B Van der Schueren at Department of Endocrinology, University Hospitals Leuven, Herestraat 49, 3000 Leuven, Belgium; Email: bart.vanderschueren{at}uzleuven.be)
Abstract
The new incretin-based therapies, dipeptidyl peptidase-4 (DPP4) inhibitors and glucagon like peptide 1 (GLP1) receptor agonists are widely used for the treatment of type 2 diabetes because of their glucose-lowering capacity with low risk of hypoglycemia. As they are weight neutral or induce weight loss in this mostly overweight population, they are popular among clinicians and patients alike. Nonetheless, concerns have been raised about GLP1's trophic effects. While increased β cell mass observed in rodents sounds appealing for treatment of diabetes, there was also an increased incidence of medullary thyroid cancer (MTC) in some species. We reviewed literature available in the Medline database until March 2012. Safety signals have emerged for MTC and pancreatic carcinoma from adverse event databases in the United States and Europe. Considering the relatively short duration of these studies, it is more likely that premalignant lesions are stimulated in presence of GLP1, rather than new neoplasms induced. Moreover, interpreting results of animal studies is difficult because of species-specific differences in presence and density of GLP1 receptors. Furthermore, data are emerging suggesting beneficial effects of GLP1 on colon and breast cancer. In conclusion, presently, the benefits of using DPP4 inhibitors or GLP1 receptor agonists for treatment of type 2 diabetes outweigh the risks. Nonetheless, their safety profile should be monitored and their indications should be widened cautiously. At present they remain contra-indicated in patients with a personal or family history of MTC or multiple endocrine neoplasia type 2.
- Revision received 29 May 2012
- Accepted 11 June 2012
- Made available online as an Accepted Preprint 12 June 2012
- © 2012 Society for Endocrinology