ArticleScientific reports2025
Insights into GLP-1 and insulin secretion mechanisms in pasireotide-induced hyperglycemia highlight effectiveness of Gs-targeting diabetes treatment.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- From glycemic control to neuroprotection: alogliptin as a repurposed candidate for Huntington's disease.Metabolic brain disease · 2026Review
- The role of growth hormone in metastasis and angiogenesis of breast cancer.Bioscience reports · 2026Review
- Berberine: A Rising Star in the Management of Type 2 Diabetes-Novel Insights into Its Anti-Inflammatory, Metabolic, and Epigenetic Mechanisms.Pharmaceuticals (Basel, Switzerland) · 2025Review
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Authors and funding
9 authors.
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Abstract
Pasireotide frequently causes severe hyperglycemia; however, its detailed mechanism remains unknown. There are no published guidelines regarding the optimal management of pasireotide-induced hyperglycemia based on its pathophysiology. Herein, we successfully switched a patient with acromegaly from a dipeptidyl peptidase-4 (DPP-4) inhibitor to a glucagon-like peptide-1 (GLP-1) analog due to pasireotide-induced deterioration of glycemic control, and we examined the underlying mechanism for glycemic control. An in vitro study was conducted using pancreatic β-cell line, MIN-6, stably expressing GLP-1R (GLP-1R-MIN-6 cells) and intestinal L-cell line, GLUTag. High glucose levels and Gs-coupled receptor stimulation synergistically triggered insulin and GLP-1 secretion. Gs-coupled receptor stimulation primarily triggered GLP-1 secretion, which was amplified by high glucose levels in GLUTag cells. Pasireotide drastically inhibited GLP-1 secretion induced by Gs-coupled receptor stimulation through SSTR5-Gi-dependent inhibition of cAMP levels, suggesting that the main pathway was completely blocked. Furthermore, administering GLP-1 partially overcame the inhibitory effect of pasireotide in GLP-1R-MIN-6 cells, leading to a partial recovery of insulin secretion. The drastic inhibition of GLP-1 secretion via shutdown of the main pathway is the primary cause of pasireotide-induced hyperglycemia. GLP-1 analogs, rather than DPP-4 inhibitors, can spare pasireotide-induced depletion of endogenous GLP-1 and restore insulin secretion.
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