In the pancreas, different types of beta cells produce insulin, which helps regulate blood sugar. According to researchers at Weill Cornell Medicine, the loss of a particularly productive type of beta cell can contribute to the development of diabetes. dr James Lo, associate professor of medicine at Weill Cornell Medicine, and colleagues measured gene expression in individual mouse beta cells to determine how many different types of beta cells are in the study, published March 16 in Nature Cell Biology exist 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 can contribute to type 2 diabetes. “Previously, people thought a beta cell was a beta cell and they just counted the total number of 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 and a cardiologist at NewYork-Presbyterian/Weill Cornell Medical Center.
“But this study tells us that it may be important to subtype the beta cells and that we need to investigate the role of these particular cluster 1 beta cells in diabetes.” dr Doron Betel, Jingli Cao, Geoffrey Pitt, and Shuibing Chen of Weill Cornell Medicine met with Dr. Lo teamed up to conduct the study. The researchers used a technique called single-cell transcriptomics to measure all of the genes expressed in individual mouse beta cells, and then used that information to group them into four types.
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The 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 fuel them to secrete more insulin. Furthermore, they were able to distinguish the cluster 1 beta cells from the other beta cell types by their high expression of the CD63 gene, which allowed them to use the CD63 protein as a marker for this specific beta cell type.
“CD63 expression gave us a way to identify the cells without destroying them and allowed us to study the living cells,” he said. When the team examined both human and mouse beta cells, they found that cluster 1 beta cells with high CD63 gene expression produce more insulin in response to sugar than the other three types of beta cells with low CD63 expression. “They are very efficient beta cells,” said Dr. Lo.
“We think they carry most of the workload for insulin production, so losing them could have profound implications.” In mice fed an obese, high-fat diet and in mice with type 2 diabetes, the number is of these insulin-producing powerhouse beta cells. “Because the number of cluster 1/high CD63 cells has decreased, you may have lower insulin production, which may play an important role in the development of diabetes,” he said.
By transplanting beta cells with high CD63 production into mice with type 2 diabetes, their blood sugar levels were returned to normal. But removing the transplanted cells caused blood sugar levels to rise again. Transplantation of low CD63-producing beta cells into the mice did not restore blood sugar to normal levels. Instead, the transplanted low CD63-beta cells appeared to be dysfunctional.
The discovery could have important implications for the use of beta cell transplants to treat diabetes, said Dr. Lo. For example, it may be better to transplant only high CD63 beta cells. He noted that it might also be possible to transplant fewer of these highly productive cells. The team of dr. Lo also found that people with type 2 diabetes had lower levels of high CD63 beta cells compared to people without diabetes.
Next, Dr. Lo and his colleagues are finding out what happens to the high CD63-producing beta cells in mice with diabetes and how to prevent them from disappearing. “If we can figure out how to keep them longer, survivable, and functioning, 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 might also be a way to get the low CD63-producing beta cells to work better,” said Dr. Lo.
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