"Although the detailed mechanism for the stimulation of intra-islet GLP-1 secretion remains to be elucidated and further studies are required, as far as we know, our present study is the first to report the effect of Oxt on inducing intra-islet GLP-1 secretion."
BUFFALO, NY — June 17, 2025 — A new research paper was published in Aging (Aging-US) Volume 17, Issue 5 , on May 1, 2025, titled " Oxytocin modulates insulin and GLP-1 secretion in pancreatic islets ."
In this study, scientists from Fukushima Medical University School of Medicine investigated how the hormone oxytocin (Oxt) influences insulin levels by acting on specific cells in the pancreas. The team led by first author Kasumi Hattori and corresponding authors Kenju Shimomura and Yuko Maejima discovered that oxytocin may indirectly increase insulin secretion by triggering another hormone, GLP-1, from within the pancreas. This finding could lead to new strategies for improving blood sugar control in people with diabetes.
Oxytocin is commonly known for its roles in childbirth and social bonding, but scientists have also been exploring its effects on metabolism. While previous studies offered mixed results about whether oxytocin raises or lowers blood sugar, this research brings new clarity. The study focused on oxytocin's impact on insulin and a hormone called GLP-1, which helps regulate insulin production. Researchers tested this by using mice with and without oxytocin receptors and found that oxytocin's ability to raise insulin levels depended on the presence of these receptors and high blood sugar conditions.
Researchers found that oxytocin stimulates the release of "intra-islet GLP-1," a form of GLP-1 produced inside the pancreas rather than the intestine. In the pancreas, insulin is produced by beta cells, while alpha cells produce glucagon, a hormone that raises blood sugar. But recent research, including this study, has shown that alpha cells can also release GLP-1, which in turn helps beta cells secrete insulin. Oxytocin appears to increase this internal GLP-1 release, especially when blood sugar levels are high, thereby leading to insulin release in a natural and targeted way.
In this study researchers were also able to detect the difference between oxytocin's effect on blood sugar and its effect on insulin. They observed that right after oxytocin was given, blood sugar levels rose in all mice—even in those that lacked oxytocin receptors. However, only the mice with working oxytocin receptors showed a later increase in insulin. This suggests that oxytocin may trigger insulin production through a separate, receptor-dependent pathway involving the hormone GLP-1.
"WT mice showed a significant increase in insulin levels at 15-min, while OxtR KO mice did not."
This indirect action—oxytocin triggering alpha cells to release GLP-1, which then acts on beta cells—may represent a novel mechanism for controlling insulin release. It also explains why oxytocin does not increase insulin in low-glucose conditions, making it a potentially safer option for regulating blood sugar.
As treatments for type 2 diabetes increasingly focus on GLP-1–based drugs, this study opens the door to using oxytocin or similar compounds to naturally enhance the body's own insulin-producing system. With further research, this mechanism could help develop new therapies that better mimic the body's natural glucose control, particularly beneficial for older adults with diabetes.
Read the full paper: DOI: https://doi.org/10.18632/aging.206244
