Aging and Beta Cells

Patient Expert

Does having type 2 diabetes destroy your beta cells?

It does in the classic explanation of type 2 diabetes progression. According to this theory, you gain too much weight for some reason or other. The increased weight causes insulin resistance (IR). The IR means you have to produce more insulin than normal to keep your blood glucose (BG) levels in the normal range. Producing all that extra insulin eventually "wears out" or "exhausts" your beta cells, so you can't produce enough insulin for the food you eat, and your BG levels start going up until you're diagnosed as diabetic.

Beta cell function also commonly declines as we age, presumably for the same reason. The beta cells get exhausted from a lifetime of producing insulin.

But a new paper  suggests that the beta cells in aged beta cells are just fine, still capable of producing insulin in response to glucose. It's the vasculature (blood vessels) surrounding the beta cells that are the problem.

When the researchers, who kindly sent me the full text of the paper, put "exhausted" beta cells from old mice into the anterior chamber of the eyes of young mice, the beta cells were rejuvenated and, with time, produced insulin like young beta cells.

Although they did not do a similar experiment with human beta cells, they said that insulin secretion from isolated old human islets (the structures that contain the beta cells) was not significantly different from that of young islets, and beta cell mass seemed to be preserved. However the blood vessels in islets from the old human donors showed signs of inflammation and fibrosis. This was more marked in islets from elderly people with diabetes.

Thus they suggest that focusing treatment on inflammation and fibrosis in the blood vessels might be the best treatment for type 2 diabetes, which usually, although not always, occurs when we're older.

So what does this research mean for us? Well, for one thing, most research, especially research that contradicts generally accepted theories, isn't usually accepted until it's been shown in other labs.

So it won't mean much to us in the short term. But in the long term, it's encouraging. If our beta cells are still OK, it means that eventually scientists could remove some beta cells and transplant them to another part of the body with good circulation, and they'd start producing insulin normally again. Removing beta cells without damaging the pancreas is not easy. But neither is brain surgery.

Because they would be our own cells, there wouldn't be any immune response. The immune attack against foreign tissue is what keeps scientists from transplanting beta cells from other people, or animals, into people with type 1 diabetes. They're trying to "encapsulate" them to keep them safe, but this technique hasn't yet been perfected.

What I find especially interesting about this research is that it suggests why controlling BG levels doesn't have as dramatic an effect on macrovascular complications (heart attacks and strokes) as it does on microvascular complications (retinopathy [eyes], neuropathy [nerves], and nephropathy [kidneys]).

Maybe diabetes doesn't cause vascular disease but vascular disease causes diabetes. In other words, the damage to the vascular system (the inflammation and fibrosis) precedes the damage to the beta cells.

If this is true, it will provide inspiration for researchers to approach control of both diabetes and vascular disease in new ways, which should doubly benefit those of us with type 2 diabetes, as most of us will eventually succumb to vascular disease.

New ideas often result in new approaches to controlling a disease that are more effective than the old approaches. Hence these new ideas about beta cells are exciting. Let's hope they lead to a treatment we can use.