Has pancreatic damage from glucagon suppressing diabetes drugs been underplayed?BMJ 2013; 346 doi: https://doi.org/10.1136/bmj.f3680 (Published 09 June 2013) Cite this as: BMJ 2013;346:f3680
- Deborah Cohen, investigations editor
- 1BMJ, London WC1H 9JR, UK
They’ve been touted as the “new darlings of diabetes treatment”—the biggest breakthrough since the discovery of insulin nearly a hundred years before. The so called incretin therapies—glucagon-like peptide-1 (GLP-1) agonists and dipeptidylpeptidase-4 (DPP-4) inhibitors—looked as if they might change the face of type 2 diabetes. Their dual action of switching on insulin and suppressing glucagon to help control blood glucose was the ultimate in diabetes care.
The promise of a Nobel prize for the investigators loomed large. Scientists had discovered a treatment that could potentially modify disease progression. Studies in experimental animals showed that GLP-1 caused a proliferation in new insulin producing β cells. The hope was that these new cells might be able to replace those that died off in the course of human diabetes.
Nor did the promise end there. GLP-1 acts on the brain to makes people feel less hungry and the more powerful drugs aid weight loss—rather than weight gain like many antidiabetic drugs before them.
It’s an effect companies are seeking to market in its own right. Spurred on by the US Food and Drug Administration’s willingness to license new obesity treatment, Novo Nordisk’s chief science officer Mads Krogsgaard Thomsen said last year that the “political establishment in the US now knows that behaviour change alone is not enough.”1
His company’s drug, liraglutide, is in the process of late stage clinical tests, which Thomsen says show promising results.
But an investigation by the BMJ suggests Thomsen’s confidence might be …
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