Overview

• The peer-reviewed study, led by Jonathan Campbell, PhD, appears in Science Advances.
• Researchers used a high-specificity mass spectrometry assay to detect only bioactive GLP-1 in pancreatic tissue from mice and humans spanning varied ages, body weights, and diabetes statuses.
• In mouse experiments, suppressing glucagon production via PC2 inhibition increased PC1 activity, elevated pancreatic GLP-1, improved glucose control, and amplified insulin secretion.
• When both PC1 and PC2 were deactivated, insulin secretion fell and blood sugar rose, confirming GLP-1’s central role in islet signaling.
• The findings challenge the gut-only view of GLP-1 production and suggest future therapies could aim to boost endogenous pancreatic GLP-1, with clinical translation still unproven and requiring further study.