In the pancreas, different types of beta cells produce insulin, which helps regulate blood sugar. Losing a specific productive type of beta cell may contribute to the development of diabetes, according to researchers at Weill Cornell Medicine.
Dr. James Lo, associate professor of medicine at Weill Cornell Medicine, and colleagues measured gene expression in individual beta cells collected from mice, published March 16 in Nature Cell Biology, to determine how many types of beta cells there are. In the pancreas. The researchers discovered four different beta cell types, one of which stood out. Cluster 1 beta cells produced more insulin than other beta cells and appeared to be better at metabolizing sugar. The study also found that the loss of these beta cells may contribute to type 2 diabetes.
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“Before this, people thought of a beta cell as a beta cell, and they just counted total beta cells,” said Dr. Lo, who is also a member of the Weill Center for Metabolic Health and the Cardiovascular Research Institute at Weill Cornell Medicine. Cardiologist at NewYork-Presbyterian/Weill Cornell Medical Center. “But this study tells us that beta cell subtyping may be important and we need to study the role of these particular cluster 1 beta cells in diabetes.”
Dr. Dr. Doron Betel, Jingli Cao, Geoffrey Pitt and Shuibing Chen to study at Weill Cornell Medicine. Worked closely with Lo.
The researchers measured all the genes expressed in individual mouse beta cells using a technique called single-cell transcriptomics and then used that information to group them into four types. Cluster 1 beta cells had a unique gene expression signature that included high expression of genes that help cellular powerhouses called mitochondria break down sugar and secrete more insulin. Additionally, they could distinguish cluster 1 beta cells from other beta cell types by their high expression of the CD63 gene, which enabled them to use the CD63 protein as a marker for this specific beta cell type.
“CD63 expression gave us a way to identify cells without destroying them and allowed us to study living cells,” he said.
When the team looked at both human and mouse beta cells, they found that cluster 1 beta cells with high CD63 gene expression produced more insulin in response to sugar than the other three types of beta cells with low CD63 expression.
“They are very high-functioning beta cells,” Dr. Lo said. “We think they carry a lot of the workload of producing insulin, so their loss could have a profound effect.”
When mice were fed an obesity-inducing, high-fat diet and mice with type 2 diabetes, the number of these insulin-producing-powerhouse beta cells decreased.
“As the number of cluster 1/high CD63 cells decreases, you can have less insulin production, which can play a big role in the development of diabetes,” he said.
Transplanting beta cells with high CD63 production into mice with type 2 diabetes returned their blood sugar levels to normal. But removing the transplanted cells brought back the high blood sugar. Transplantation of low CD63-producing beta cells into mice did not return blood sugar levels to normal levels. Transplanted low CD63 beta cells appeared rather inactive.
This discovery may have important implications for the use of beta cell transplants in the treatment of diabetes, Dr. Lo said. For example, it may be better to transplant only high CD63-beta cells. He noted that it might even be possible to transplant a few of these highly productive cells. Dr. Loco’s team also found that people with type 2 diabetes had fewer elevated CD63 beta cells than people without diabetes.
Then, Dr. Lo and his colleagues want to know what happens to the high CD63-producing beta cells in diabetic mice and how to prevent them from disappearing.
“If we can figure out how to keep them alive and functional for a long time, it could lead to better ways to treat or prevent type 2 diabetes,” he said.
They also want to study how existing diabetes treatments affect all types of beta cells. GLP-1 agonists, which help increase insulin release in people with diabetes, interact with high- and low-CD63-producing beta cells.
“Our study also shows that GLP-1 agonists may also be a way to make low CD63-producing beta cells work better,” said Dr. Lo said.
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