Inhibiting the hormone somatostatin could represent a promising new approach to prevent severe drops in blood glucose levels for individuals with type 1 diabetes. According to research conducted at institutions including the University of Gothenburg, this strategy may have life-saving potential.
Inhibiting the hormone somatostatin could be a promising new approach to prevent severe drops in blood glucose levels for individuals with type 1 diabetes. Research conducted at the University of Gothenburg and other institutions suggests that this method could save lives.
In healthy people, when blood glucose levels fall, the body releases glucagon, a hormone that prompts the liver to produce glucose, helping to bring blood sugar levels back to normal. Glucagon works in opposition to insulin, the hormone that reduces blood glucose levels. Both hormones are made in the pancreas.
Individuals with type 1 diabetes lack insulin and also have a deficiency in glucagon. When glucagon isn’t secreted during low blood glucose events, it can result in dangerously low sugar levels, which is responsible for about 10% of fatalities among those with type 1 diabetes.
Restored ability to prevent drops in blood sugar
The recent study, featured in the journal Nature Metabolism, introduces a potential new treatment for preventing severe drops in blood sugar for type 1 diabetes patients. One of the leading experts on this project, Patrik Rorsman, is a Professor of Cellular Endocrinology at the Sahlgrenska Academy at the University of Gothenburg and also works at the University of Oxford.
In their research, the scientists explored hormone-secreting cells from both human and mouse pancreases. They discovered that these islets are unable to secrete glucagon during episodes of low blood sugar in individuals with type 1 diabetes. This occurs because there is an increased release of somatostatin, which inhibits glucagon release.
Additionally, experiments indicated that by blocking somatostatin in mice with type 1 diabetes, researchers could restore glucagon release from the pancreas during low blood sugar situations, thereby preventing potentially life-threatening low glucose levels. This blockage was achieved through pharmacological methods.
Mapping previously unknown signaling pathways
By utilizing genetically modified mice with light-activated beta cells, a technique called optogenetics, the researchers also examined the interactions among various cell types in the pancreatic islets: the glucagon-releasing alpha cells, insulin-releasing beta cells, and somatostatin-releasing delta cells.
The findings shed light on how a decrease in functioning beta cells in type 1 diabetes is related to an increased risk of blood sugar fluctuations, an area that had been unclear until now.
Anna Benrick, an Associate Professor of Physiology at the Sahlgrenska Academy at the University of Gothenburg and a co-author of the study, stated, “These new insights reveal a crucial and previously unrecognized role of electrical signaling that occurs through direct cell connections between beta cells and delta cells.” She added, “If these electrical connections are compromised, glucagon release declines, raising the potential for blood sugar drops. The possibility of restoring this through pharmacological means by blocking somatostatin could help in preventing dangerous blood sugar fluctuations in type 1 diabetes.”
