2024-10-18 00:18:00
In patients with type 1 diabetes there is a dysregulation of glucagon secretion, which can lead to a significant drop in blood sugar levels. To prevent this type of situation, new strategies are being studied, including the inhibition of the hormone somatostatin.
People with type 1 diabetes have a deficiency of insulin, but also glucagon. Glucagon has the opposite effect on the body to that of insulin, which reduces blood sugar. Both hormones are produced in the pancreas. When glucagon is not released during a drop in blood sugar, dangerously low blood sugar levels occur, a condition that causes about 10% of all deaths in type 1 diabetes.
Faced with this type of situation, a recent study carried out by scientists from the University of Gothenburg (Sweden) and published in the journal “Nature Metabolism” suggests a potential treatment strategy based on the inhibition of the hormone somatostatin. Blocking this hormone in mice with type 1 diabetes could restore the pancreas’ ability to release glucagon when blood sugar levels are low, thus preventing dangerously low levels.
The researchers examined clusters of hormone-producing cells from the pancreases of humans and mice. They were able to show that in type 1 diabetes, these islets are unable to release glucagon when blood sugar is low. This is because the hormone somatostatin is released in greater quantities in type 1 diabetes and inhibits the release of glucagon.
The researchers looked at groups of hormone-producing cells from the pancreases of humans and mice. They were able to show that in type 1 diabetes, these islets are unable to release glucagon when blood sugar is low. This is because the hormone somatostatin is released in greater quantities in type 1 diabetes and inhibits the release of glucagon.
Hormonal hypersecretion
The study used genetically modified mice in which beta cells were activated by light, a phenomenon known as optogenetics. The interaction between different types of cells in the pancreatic islets was also mapped: alpha cells that release glucagon, beta cells that delta cells release insulin and somatostatin-releasing cells. LDB/MTT (SyM)
The results proved it Glucagon secretion is not stimulated by low glucose levels in patients’ islets with type 1 diabetes. This occurs due to hypersecretion of somatostatinleading to aberrant paracrine inhibition of glucagon secretion.
“The new findings highlight an important and previously unknown role of electrical signaling that occurs through open cellular connections between beta cells and delta cells. If the electrical connections are lost, glucagon release is reduced and the risk of a drop in blood pressure increases,” one of the co-authors explained, Anna Benrick, Associate Professor of Physiology at the Sahlgrenska Academy, University of Gothenburg.
The authors underlined, in this regard, that It is possible to pharmacologically restore this situation by blocking somatostatin.this opens up the possibility of preventing dangerous drops in blood sugar in type 1 diabetes. JGS. SJD
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