High blood sugar levels kill off beta cells, the cells in the pancreas that produce insulin. So if we have type 2 diabetes and we’ve had poor control for a long time, we probably don’t have many beta cells left.
This is the classic interpretation of diabetes progression in type 2 diabetes.
But now, new research at Columbia University has suggested that those beta cells didn’t die after all. Instead they’ve de-differentiated into progenitor cells, which like stem cells can differentiate into different cell types. Some of these progenitor cells then differentiate into alpha cells, which produce glucagon.
Glucagon does the opposite of insulin: it increases blood glucose (BG) levels instead of reducing them. And higher glucagon levels in addition to lower insulin levels magnifies the BG increase in type 2 diabetes.
In science, just one result from one lab may not be the last word. The first step is for other scientists to replicate the results to show that they’re real and just not some artifact caused by some technique used by a particular lab.
But if these results can be replicated, they’re exciting. It means that even if you’ve had type 2 diabetes for many years and don’t seem to have much remaining ability to produce your own insulin, if the scientists could figure out how to nudge these progenitor cells into differentiating into beta cells, your control would be much much better.
The authors suggest that stressing beta cells with drugs that make them produce more insulin, in other words, sulfonylureas, is not a good idea, and that resting the beta cells by injecting insulin is a better idea. Some physicians such as Richard K. Bernstein have been saying this for years. Others said sulfonylureas (which are cheap) were no worse than other drugs.
The new study suggests that Bernstein is right.
Now the challenge is for the scientists to figure out how to get those progenitor cells to redifferentiate into beta cells rather than trying to get differentiated beta cells to replicate, which has been the focus of much research.