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The Role of Beta Cell "Hubs" in Diabetes Revealed


The study confirmed a suspicion that not all beta cells are equal in regulating insulin secretion.

Beta cell failure and its role in the development to diabetes is well-known. But a new study from the University of Birmingham confirms a suspicion that not all cells are equal.

By mapping cell behavior, researchers have shown that it’s the functioning of a few key cells, which researchers call beta cell “hubs,” that determine whether diabetes occurs.

Findings in Cell Metabolism not only pinpoint the behavior of these beta cell hubs; the work also lays the groundwork for targeting these specific cells with therapy to treat the disease.

The study used optgenetic and photopharamacological targeting to build a blueprint of how the beta cell clusters function. “It has long been suspected that ‘not all cells are equal’ when it comes to insulin secretion,” said David J. Hodson, PhD, senior author on the paper.

About 65% to 80% of the cells in the islets of the pancreas are beta cells. When working correctly, these cells know when to store and when to release insulin to regulate blood glucose levels. In a person without diabetes, the beta cells are constantly making tweaks in insulin to respond to changes in the body.

But these findings show that only a smaller fraction of the beta cells—between 1% and 10%--regulate insulin and, in turn, blood glucose control. Hodson likened their role to that of a “pacemaker” for insulin secretion. “We found that when their activity was silenced, islets were no longer able to properly respond to glucose.”

The work was carrying out on both mice models and human tissue. The researchers cautioned that the studies may not reflect “in vivo” functioning. Despite this limitation, they wrote, the study “nonetheless provides a strong foundation for understanding the biology of these unusual cells.”


Johnston NR, Mitchell RK, Haythorne E, et al. Beta cell hubs dictate pancreatic islet responses to glucose [published online July 21, 2016]. Cell Metabolism, 2016; doi:10.1016/j.cmet.2016.06.020

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