I don't know about other people, but I'm getting really, really, really tired of seeing popular press articles about type 2 diabetes illustrated with photos of people pricking their fingers to get blood.
I mean, I know that unless you use a continuous glucose monitor, pricking your fingers is part of having diabetes. But it's not the only part. In fact, it's a very minor part. Controlling your diet is much more important.
But the finger jabbing seems to be a cliche for type 2 diabetes.
Another cliche I hate is that of a man and a woman, usually about 40 or 50 and trim, running along a deserted beach, intended to illustrate exercise.
I mean, I know running along a beach would be good exercise, but how many people live near a beach, especially a deserted beach like the ones always shown? And if they were just diagnosed with type 2 diabetes, how many would be slim and trim like the models? Maybe some, but not the majority.
Finally, the last cliche is the same attractive couple that was running along the beach preparing a salad in a perfectly appointed kitchen while grinning from ear to ear. "Diabetes is such fun! We can't wait to finish this delicious salad so we can go out to the beach again for some more running. If it's rainng, we can stay home and do some finger-pricking to prove we're really diabetic."
OK. I'm in a bad mood. I couldn't find a deserted beach and I ran out of salad fixings. Maybe tomorrow someone will come up with some more interesting popular-press illustrations.
Sunday, June 30, 2019
Thursday, June 27, 2019
Pancreatic Islet "Leader" Cells
No one understands yet exactly what regulates the release of insulin from the beta cells in the pancreas. We just know that the process is disrupted when you have diabetes, almost completely in the case of type 1 diabetes and partially when you have type 2.
Now researchers in several countries, including Germany, Great Britain, Canada, and Italy, have discovered a new clue. It seems that certain beta cells are "leader" cells or "hub" cells, and they control the other beta cells. This is like the heart's sinoatrial node (called the "pacemaker of the heart"), which controls the beating of other heart cells. And some researchers refer to the leader cells in the pancreas as pacemakers.
The studies show that if you selectively delete the leader cells in animal models of diabetes, the response to glucose becomes disrupted. It is known that in type 2 diabetes, the normally regular pulses of insulin that occur even when fasting are lost. Could this be because the leader cells are damaged? If so, why are they damaged? Are they more sensitive to high glucose and other toxins than the other beta cells?
The researchers found that the coordination of responses controlled by the leader cells was impaired in human islets taken from subjects with diabetes.
This is all fascinating albeit early days. This new study doesn't have any practical utility yet, but it could lead to more research that would have practical application.
If the heart's pacemaker isn't working well, they can give you an artificial pacemaker. The beta cell pacemakers wouldn't be as easy to replace. But perhaps now that it's known that there are such pancreas pacemakers, someone will figure out how to rejuvenate them.
Now researchers in several countries, including Germany, Great Britain, Canada, and Italy, have discovered a new clue. It seems that certain beta cells are "leader" cells or "hub" cells, and they control the other beta cells. This is like the heart's sinoatrial node (called the "pacemaker of the heart"), which controls the beating of other heart cells. And some researchers refer to the leader cells in the pancreas as pacemakers.
The studies show that if you selectively delete the leader cells in animal models of diabetes, the response to glucose becomes disrupted. It is known that in type 2 diabetes, the normally regular pulses of insulin that occur even when fasting are lost. Could this be because the leader cells are damaged? If so, why are they damaged? Are they more sensitive to high glucose and other toxins than the other beta cells?
The researchers found that the coordination of responses controlled by the leader cells was impaired in human islets taken from subjects with diabetes.
This is all fascinating albeit early days. This new study doesn't have any practical utility yet, but it could lead to more research that would have practical application.
If the heart's pacemaker isn't working well, they can give you an artificial pacemaker. The beta cell pacemakers wouldn't be as easy to replace. But perhaps now that it's known that there are such pancreas pacemakers, someone will figure out how to rejuvenate them.
Monday, June 3, 2019
Helping Beta Cells
Two recent research reports concern helping beta cells produce more insulin. Interestingly, they both involve inhibiting something rather than trying to stimulate the beta cells, as the sulfonylurea drugs do.
People think of type 2 diabetes as being caused by insulin resistance and some wonder why you would want to produce more insulin if you have type 2. But in fact, type 2 is often caused by insulin deficiency. That is, you're producing insulin, often more than normal, but it's not enough to overcome your insulin resistance. So more insulin can help.
The first study involves deleting senescent, or old, beta cells from the pancreas. When the Joslin Diabetes Center researchers did this in mice, they found that the remaining beta cells were rejuvenated and started producing enough insulin to keep blood glucose (BG) levels in the normal range.
How did they do this? One approach was genetic modification, which is fine in mice but unlikely to be practical in humans. The other approach was with senolytic drugs, drugs that remove senescent cells. Although you can buy drugs claiming to be senolytics from companies that market supplements, this field is relatively new and large-scale controlled trials have not yet been done. Pilot studies show promise.
The authors of this paper think that diabetes is caused by stress: in type 2 the stress of insulin resistance and in type 1 the stress of an autoimmune attack. Of course this doesn't explain what causes insulin resistance or an autoimmune attack, and these are the underlying problems.
The second study involved removing two signaling molecules that dampen the insulin response. This is the opposite of most approaches, which try to stimulate the insulin response directly instead of inhibiting inhibitors. The sulfonylureas stimulate insulin release, even when a person is not eating carbohydrate, which means your blood glucose can go low when you're not eating.
These studies were done in mice, and oddly, removing the inhibitors worked only when the mice were on a high-fat diet. The reason for this is not yet known.
The inhibitors are TLR2 and TLR4. TLR stands for toll-like receptor, and normally, TLR2 and TLR4 stimulate the immune system when they detect invadors. But they also work together to block beta cell proliferation, so when you remove them, the beta cells multiply like mad, so much that they can be seen with the naked eye.
There are in fact drugs that inhibit TLR2 and TLR4, but inhibiting them would not only stimulate beta cell growth, but it would inhibit the immune system and make a person susceptible to infection.
Nevertheless these new approaches are interesting and may result in methods to rejuvenate beta cells in people with both types of diabetes (most people with type 1 do have a few beta cells remaining despite the autoimmune attack). How wonderful that would be.
a
People think of type 2 diabetes as being caused by insulin resistance and some wonder why you would want to produce more insulin if you have type 2. But in fact, type 2 is often caused by insulin deficiency. That is, you're producing insulin, often more than normal, but it's not enough to overcome your insulin resistance. So more insulin can help.
The first study involves deleting senescent, or old, beta cells from the pancreas. When the Joslin Diabetes Center researchers did this in mice, they found that the remaining beta cells were rejuvenated and started producing enough insulin to keep blood glucose (BG) levels in the normal range.
How did they do this? One approach was genetic modification, which is fine in mice but unlikely to be practical in humans. The other approach was with senolytic drugs, drugs that remove senescent cells. Although you can buy drugs claiming to be senolytics from companies that market supplements, this field is relatively new and large-scale controlled trials have not yet been done. Pilot studies show promise.
The authors of this paper think that diabetes is caused by stress: in type 2 the stress of insulin resistance and in type 1 the stress of an autoimmune attack. Of course this doesn't explain what causes insulin resistance or an autoimmune attack, and these are the underlying problems.
The second study involved removing two signaling molecules that dampen the insulin response. This is the opposite of most approaches, which try to stimulate the insulin response directly instead of inhibiting inhibitors. The sulfonylureas stimulate insulin release, even when a person is not eating carbohydrate, which means your blood glucose can go low when you're not eating.
These studies were done in mice, and oddly, removing the inhibitors worked only when the mice were on a high-fat diet. The reason for this is not yet known.
The inhibitors are TLR2 and TLR4. TLR stands for toll-like receptor, and normally, TLR2 and TLR4 stimulate the immune system when they detect invadors. But they also work together to block beta cell proliferation, so when you remove them, the beta cells multiply like mad, so much that they can be seen with the naked eye.
There are in fact drugs that inhibit TLR2 and TLR4, but inhibiting them would not only stimulate beta cell growth, but it would inhibit the immune system and make a person susceptible to infection.
Nevertheless these new approaches are interesting and may result in methods to rejuvenate beta cells in people with both types of diabetes (most people with type 1 do have a few beta cells remaining despite the autoimmune attack). How wonderful that would be.
a
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