We’ve always been told that insulin serves as a “key” to unlock our cells and enable them to get the glucose they need. Without insulin, our cells cannot function.
My mind was completely blown by this research conducted by UT Southwestern Medical Center. They suppressed the response to glucagon in mice. Then they destroyed their insulin-producing beta cells.
And… the mice did not develop diabetes. Their blood glucose levels remained normal, and their cells continued to metabolize glucose from the bloodstream. Researchers have no idea how this is occurring, but it is.
Could everything we thought we knew about diabetes be wrong?
This is … strange. I’d love to hear more about it. If it could be as simple as suppressing glucagon that WOULD change completely what we thought we knew about diabetes.
Being a T1 HUMAN for 30 years now, I’m pretty sure that the mouse experiments don’t really directly translate into human application on T1’s.
But as for suppressing the effect of glucagon in mice, that sounds very similar to what Metformin does in humans. (Read up on it… it’s primary effect is suppressing gluconeogenesis.) And Metformin is a very useful drug for T2’s.
But is Metformin a replacement for insulin in T1’s? Most certainly not.
Love this news, obviously we can’t draw conclusions yet, but it’s exciting! I hope these researchers get money to follow this fast!
So nature has invented something that is completely useless. The mechanism was passed along the evolutionary chain of mammals. To our knowledge not one mutation has occured that is independent of insulin by supressing glucagon. Is this likely in such a huge timeframe? I think the researchers have to find out about the benefits of glucagon first to draw the right conclusion. Nevertheless the finding is really remarkable.
When I first read this, my first thought was “something is missing” - I have a feeling that something was grossly overlooked in this “research”. We T1’s have impaired alpha cell function as well as beta cell destruction, which means our glucagon production is already sub-optimal… that’s why we suffer from such severe lows, it’s not JUST because we inject insulin - our bodies simply can’t regulate our BG in any reliable capacity.
Lara, maybe I’m just more cynical than you, but I’ve been T1 for 30 years now and I can tell you, several times every year they cure T1 diabetes in mice every-which-way-from-Sunday. But despite the press releases, I don’t see how it’s helped me any.
I’m not opposed to research in mice or whatever. It’s just that I don’t see how it’ll ever help me. (Maybe somebody else).
This is basic research which is always a long way from clinical research. I noted a key point that does make a difference in how you read this. "The researchers, from UT Southwestern Medical Center, used mice that have been specially bred not to respond to glucagon, . . . .
It may help in understanding their questions (not included in the abstract) but I never get too excited about a single study.
This is not the first time “Type 1 diabetes” has been cured in mice without insulin. It’s also true that Type 1 has been cured in mice several dozen times over (no exaggeration), and that the vast majority of these cures end up not working for humans. A big part of the problem is that the mice themselves don’t actually have Type 1 diabetes, but are genetically engineered to have their beta cells die early on in life.
Also, in regards to Sarah’s comment about glucagon: It’s my understanding that Type 1s actually do produce adequate amounts of glucagon, or at least have the potential to do so. In fact, we produce too much glucagon a majority of the time, most especially after meals (this is one of the things amylin/Symlin helps suppress thus leading to improved postprandial BGs), but in the case of lows we produce too little too late. It’s not that we can’t produce it, just that our bodies are all screwed up in the timing of it, giving us too much when we don’t need it and too little when we actually do. I would guess this probably has a lot to do with the fact that glucagon secretion is controlled by insulin levels in the blood, and a Type 1s insulin levels are virtually never normal. Although this doesn’t really explain why Type 2s don’t have such impaired glucagon secretion in response to lows, so maybe I’m missing something.
I agree with Tim. I do read the research, but I only get excited about research when it reaches the human-testing phase …
Tim, I’ve been T1 35 years and I hear your frustration! But this study gave a result that goes against everything we thought was true.
Just to clarify to some of the other posters, the team did not alter how the mice produce glucagon. They altered the glucagon receptors in the cells. So the glucagon was still being produced, but the cells would not respond to it. That’s how I read it, anyway! 
Here’s a really good articlethat talks about the study.
Well, it’s just not that simple. What the researchers didn’t tell you is that mice replace missing beta cells VERY quickly – as much as 10 times faster than humans do. (Yes, Type 1’s do grow new beta cells, but the autoimmune attacking T-cells are just sitting there ready to kill them off again). So I doubt these mice were without insulin for very long, because they DIDN’T have any auto-immune component. This seems to me to be a trash study and a gross waste of money.
The study was funded mainly by NIH and ADA.
Saw this. Even if not entirely true, maybe Leptin can be used to reduce the need for insulin, so you are using a lot less. Paper mentioned something like a 90 percent reduction. This would be great, as I am not a big fan of babysitting insulin dosages… could make life a lot easier.