I saw this online this morning, so I decided to share it with the rest of you.
“In a world-first medical breakthrough, scientists in Sweden and the United States have successfully used CRISPR gene-editing to reprogram pancreatic islet cells so they can evade immune rejection after transplantation — a revolutionary advance in diabetes treatment.
By modifying three critical genes — two to reduce immune detection and one to add a protective “don’t eat me” signal (CD47) — researchers made the transplanted cells effectively invisible to the immune system. When implanted into the forearm of a man with Type 1 diabetes, these cells began producing insulin naturally, without the need for lifelong immunosuppressive drugs.
This marks the first time a human has regained natural insulin production through gene-edited cells — shifting the future of diabetes care from constant management to the possibility of a functional cure. While the patient still needs minimal insulin support, experts believe this innovation could soon help millions live insulin-free lives, transforming hope into healing.
As we long-time diabetics know, the promise of a “cure” in our lifetimes must be taken with great doubt, but this does SEEM to be a step in the right direction.
This does seem to be a credible possibility of a cure, @SherryAnn. Thanks for posting this. Its credibility is enhanced since it was actually tested on a human T1D, not a mouse!
My thoughts exactly, Terry4. Certainly this process will not work for everyone – including me since I already must take an immunosuppressant drug for Dermatomyositis – but I sincerely hope that this line of research will someday soon be helpful to others.
I think at this point it is a possibility of a treatment. A cure requires fully functioning beta cells in the islets, adjacent to the alpha cells; without that we will still have an impaired glucagon response.
I’ve made the point before and I’ve asked my endo whether he knows of anything (no response) but simply having an AIDS which delivers directly into the major blood supply, ideally the portal vein (which connects the pancreas and other organs to the liver) would make an AIDS almost “perfect”.
An implanted system which delivered into the islets would apparently solve the glucagon problem too.
Of course as with any AIDS many of the metabolic controls that beta cells implement would be missing; an AIDS only responds to BG (at present), not things like stress, hunger, anticipated food intake, critically low blood sugar (though that’s probably not the beta cells).
I just don’t understand why there isn’t more research on this. It seems as though the medical community as a whole has poor vision of viable yet mechanical approaches, solutions even.
That subscription is a bit rich for me. What I would like to know are they replicating complete islets with all cell types because they all interact with each other but only to hormones secreted within the islets. As @John_Bowler said this is the only way to gain complete glucose control. Many with T1 and T2 have poor functioning Alpha cells causing poor response to hypoglycemia.
They’re creating beta cells that have been GMed to evade our natural immune systems.
Their assumption is that those cells have the same metabolic responses to any stimuli they receive as aboriginal beta cells.
The problem is that by injecting them into human arms the various metabolic responses may be delayed or ineffective and the neogenic beta cells own metabolic stimuli may, also, be delayed or ineffective.
My refutation of the approach is based on peer-reviewed research that the beta cell metabolic control is at least partly based on physical proximity.
That doesn’t mean the research is either invalid or unuseful. Rather it means the marketing hyperbole is. The journalists do not explain context and fail to understand reality. We do.
I’m starting to believe that the complexity of what goes on is beyond human comprehension. I based my comment on a paper I had read that simply explored what happened to alpha-cells glucagon production in response to insulin in vitro. The paper hypothesised that the concentrations required to stop glucagon production could only be achieved by the close proximity within the islet cells.
That may be simplistic and the complexity is, I suspect, to the point that it is beyond human comprehension.
Human comprehension is limited in scope; I’m trained in Chemistry but even within that field my understanding is limited. I cannot understand, let alone explain, even the Chemistry I know it terms of Physics.
I believe we have reached this limit in Diabetes; we are fundamentally unable to understand it, so explaining it is, well…
Traditionally we have approached this by divide-and-concur. Ab initio western understanding started with the “natural sciences”, i.e. the stuff other than the god stuff.
Somehow someone invented the required subdivision; the natural sciences were subdivided into pieces that could exist together despite not affirming each other (paraphrasing “Godel, Escher, Bach” and with no greater validity).
I don’t believe that human metabolism can be subdivided at this point; I’m simply saying we have reached the end of the abstraction. We have learned all that we can from the approach.
Nothing I’ve read on this process has made it clear what is meant by Islets. It appears that these are Islets with only one cell type, Beta. True Islets of Langerhans have 5 cell types that secrete 6 homones.
The endocrine system is so interrelated. This is absolutely true of the glucose regulatory hormones secreted by the cells in the Islets of Langerhans. These 5 cdell types have receptors that trigger or repress secretion of homones.
As @John_Bowler wrote, it is complicated, but I think that we, including the scientific community can grasp the idea that the cells in the islets are a community that are in constant conversation with each other through their various hormones.
If my hypothesis that Beta cell insufficiency in the pancreatic islets cause more than hyperglycemia due to lack of insulin, but also cause poor Alpha cell response to hypoglycemia. This is the simlpest interaction between the 5 endocrine cell types in the Islets.
I applaud this advance in working towards a cure for T1DM. I just don’t think it goes far enough if the islets only contain Beta cells. If enough of these islets are transplanted to not need exogenous insulin, I suspect that there will be problems with hypoglycemia.
I’m with you that I want my full pancreatic islet cell metabolic system restored. I always thought in autoimmune diabetes only the beta cells are destroyed so a cell replacement therapy would only have to replace the beta cells?
The problem is getting them into the islets. The stuff I have seen puts beta cells into other places, like the liver. The existing research suggests, very strongly, that this won’t fix the impaired glucagon response because that requires close proximity; the beta cells have to be in the islets along side the alpha cells to shut down the alpha cell glucagon production.
It’s not clear how long a beta cell which is continuously producing insulin to counter the liver’s release of glucose is going to keep going. It’s not clear to me how well a beta cell at such a remote location will handle all the other metabolic control pathways.
It’s certainly not clear what the term “islet cells” means. I didn’t read the full text as it means at least signing up to the web site to get “free access”, I’ve no doubt that makes things more clear but the Science article says:
The company is now pursuing a slightly different strategy that involves genetically engineering beta cells grown in culture from stem cells, which are easier to obtain in large numbers than donated beta cells
So it sounds like “islet cells” and “pancreatic cells” are both being used to mean “beta cells”. The same semantic problem exists with the concept of “islet transplantation”, which should, apparently, mean complete islets but that’s not clear either.
Most people don’t know what beta cells are or, for that matter, islet cells. We’re not talking about “most people” here, we’re talking about medical researchers in the field who certainly do know. The Science article apparently translated “islet” to “pancreas”, which is sort of ok give than Science is a mass market publication; “islet” is being used in a very specific way (like it means something different in geography and so on.)
The ADA definition of major organ failure is something that is (now) considered a disability, but failure means a loss of functionality in this context, not complete absence and ADA defines it as something that has a substantial effect on ability to do things.
So it is correct on several levels to say that something is broken when it is not capable of performing at least one of it’s essential actions. For example I might say my car is broke if the driver seatbelt has sheared through; I can still drive it but I would be breaking the law if I did. I might also say it was broke if one of the tires was deflated but then I could just pump it up or swap it out for the spare; there is something I could do in the moment to fix it so it’s not really broken, I just can’t be bothered to fix it.
