New Strategy to Prevent Hypoglycemia in Type 1 Diabetes: Targeting Somatostatin

A recent study from the University of Gothenburg suggests that inhibiting somatostatin, a hormone found in the pancreas, may prevent life-threatening blood sugar drops in people with type 1 diabetes. The research, published in Nature Metabolism, uncovers a novel approach that could potentially save lives by restoring the body's ability to regulate blood glucose levels during hypoglycemia.

In type 1 diabetes, the body’s ability to release glucagon, a hormone that raises blood glucose levels when they drop too low, is impaired. Typically, glucagon helps counterbalance the effects of insulin, which lowers blood sugar. However, individuals with type 1 diabetes not only lack insulin but also struggle to release glucagon during hypoglycemia, leading to dangerously low blood sugar levels—a condition responsible for about 10% of deaths in this population. Researchers discovered that elevated levels of somatostatin inhibit glucagon release, worsening this problem.

The new study provides promising evidence that pharmacologically blocking somatostatin could restore glucagon release in the pancreas. Using a mouse model, the researchers demonstrated that inhibiting somatostatin allowed glucagon release during hypoglycemia, effectively preventing severe blood sugar drops. This breakthrough identifies a crucial mechanism linking somatostatin to glucagon deficiency and suggests a potential therapeutic target for preventing hypoglycemia in type 1 diabetes.

The findings hold significant clinical implications. Hypoglycemia is a leading cause of morbidity and mortality in type 1 diabetes, and current treatments mainly focus on insulin management without adequately addressing glucagon release. By focusing on somatostatin inhibition, this approach could offer a new strategy to improve glucose regulation and reduce the risks associated with hypoglycemia, improving outcomes for individuals with type 1 diabetes.