Beta cells in the pancreas are critical as they produce insulin, which aids in the regulation of blood sugar levels.
However, a study by Weill Cornell Medicine has revealed that not all beta cells are identical, and the loss of a certain type can contribute to the onset of diabetes.
Different Types of Beta Cells
In the study, published in Nature Cell Biology, Dr. James Lo and his team identified four distinct types of beta cells.
They found that one specific type, referred to as cluster 1 beta cells, produced more insulin and metabolized sugar more efficiently than the other three types.
The loss of these specific cells could contribute to type 2 diabetes. The study highlights the need to differentiate between beta cell types, emphasizing the significance of cluster 1 cells in relation to diabetes.
The Study and its Techniques
The research team used single-cell transcriptomics, a technique that allowed them to measure all the genes expressed in individual mouse beta cells.
They categorized the cells into four types. Cluster 1 beta cells were unique, demonstrating high expression of genes that aided in sugar breakdown and insulin secretion.
These cells also showed high expression of the CD63 gene, making CD63 protein a marker for this particular beta cell type.
Findings in Mice and Humans
Both human and mouse beta cells that demonstrated high CD63 gene expression produced more insulin in response to sugar.
Obese mice and mice with type 2 diabetes saw a decrease in the number of these high-performing beta cells. This decrease could lead to lower insulin production and contribute to diabetes development.
Implications for Treatment
When the researchers transplanted high CD63-producing beta cells into diabetic mice, their blood sugar levels normalized. The removal of these cells led to a return of high blood sugar levels.
Transplanting beta cells with low CD63 production did not produce the same effect. This discovery may prove crucial for diabetes treatment, particularly for beta cell transplants.
It could be more effective to transplant high CD63 beta cells and might even be possible to transplant fewer of these high-performing cells.
Future Research
The team plans to investigate why high CD63-producing beta cells decrease in diabetic mice and how to prevent this loss. If these cells can be kept functional, it could lead to improved methods to treat or prevent type 2 diabetes.
The team also intends to examine how current diabetes treatments impact different types of beta cells, particularly in relation to GLP-1 agonists, which increase insulin release in people with diabetes.
The study was published in Nature Cell Biology. For further information, please consider reading other studies about diabetes, whole grain foods, and blood sugar control.
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