This record provides bibliographic details and links to the original research. An editorial study breakdown is not available.
What the researchers found
Pasireotide caused severe blood sugar problems mainly by shutting down GLP-1 secretion. A GLP-1 analog worked better than a DPP-4 inhibitor to restore insulin release in both a patient and cell models.
Why it matters
Pasireotide treats acromegaly but often causes hard-to-manage high blood sugar. This study clarifies why and suggests GLP-1 analogs as the better treatment choice.
The numbers in context
One patient with acromegaly switched from DPP-4 inhibitor to GLP-1 analog. In vitro: pasireotide blocked GLP-1 secretion via SSTR5-Gi pathway. GLP-1 partially restored insulin secretion in GLP-1R-MIN-6 cells.
How the study worked
Clinical case of drug switching plus in vitro experiments using MIN-6 beta cells stably expressing GLP-1R and GLUTag intestinal L-cells. Tested interactions between glucose, Gs-coupled receptor stimulation, and pasireotide.
Who was studied
One acromegaly patient; pancreatic beta cell and intestinal L-cell lines
What this study cannot tell us
Single patient case. Cell line results may not fully reflect human physiology. No controlled clinical trial.
Read the original research
Insights into GLP-1 and insulin secretion mechanisms in pasireotide-induced hyperglycemia highlight effectiveness of Gs-targeting diabetes treatment.
Scientific reports, 15(1), 9494
Citation
Sato, Junichiro; Manaka, Katsunori; Horikoshi, Hirofumi; Taguchi, Maho; Harada, Kazuki; Tsuboi, Takashi; Nangaku, Masaomi; Iiri, Taroh; Makita, Noriko. (2025). Insights into GLP-1 and insulin secretion mechanisms in pasireotide-induced hyperglycemia highlight effectiveness of Gs-targeting diabetes treatment.. Scientific reports, 15(1), 9494. https://doi.org/10.1038/s41598-025-90896-2