A groundbreaking study from the University of Gothenburg has identified a potential new treatment for preventing dangerous drops in blood glucose levels for individuals with type 1 diabetes. Researchers propose that inhibiting the hormone somatostatin may significantly mitigate hypoglycemic episodes, a condition that accounts for approximately 10% of fatalities in this population.
In healthy individuals, a decline in blood glucose triggers the release of glucagon, a hormone that prompts the liver to produce glucose, thereby stabilizing blood sugar levels. This process is countered by insulin, which lowers blood glucose. Both glucagon and insulin are produced in the pancreas.
However, individuals with type 1 diabetes experience a dual deficiency of insulin and glucagon. The absence of glucagon release during hypoglycemic events can lead to critically low blood sugar levels, resulting in severe health complications.
Restoration of Glucagon Release
The research, published in the journal Nature Metabolism, sheds light on a novel treatment approach aimed at counteracting life-threatening blood sugar dips. Leading the study is Patrik Rorsman, a Professor of Cellular Endocrinology at the Sahlgrenska Academy, who is also affiliated with the University of Oxford.
The study examined pancreatic islet cells—groups of hormone-producing cells—in both human and mouse subjects. Findings revealed that in individuals with type 1 diabetes, these islets fail to release glucagon in response to low blood sugar. This dysfunction is attributed to elevated levels of somatostatin, which inhibits glucagon secretion.
In experimental models, researchers demonstrated that pharmacologically blocking somatostatin in mice with type 1 diabetes restored the pancreas’s ability to release glucagon during hypoglycemic episodes, thus preventing dangerously low blood glucose levels.
Novel Signaling Mechanisms Uncovered
Using optogenetic techniques with genetically modified mice, the researchers explored the interactions among various cell types within the pancreatic islets: glucagon-releasing alpha cells, insulin-secreting beta cells, and somatostatin-producing delta cells.
These insights offer a clearer understanding of how the diminished function of beta cells in type 1 diabetes correlates with an increased risk of hypoglycemia, a connection that was previously poorly understood.
Anna Benrick, an Associate Professor of Physiology at the Sahlgrenska Academy and co-author of the study, emphasized the significance of the findings. “Our results reveal an important and previously unknown role of electrical signaling through intercellular connections between beta and delta cells. Loss of these electrical connections reduces glucagon release and heightens the risk of hypoglycemia. Importantly, our ability to pharmacologically restore this function by blocking somatostatin suggests a promising avenue for preventing severe blood glucose drops in individuals with type 1 diabetes.”
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