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Could Type 1 Diabetes Be Reversible After All?


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Type 1 diabetes is characterized by the loss of insulin-producing 𝛽 cells in the pancreas and has largely been thought to be irreversible—until now. Newly published research suggests that there might be a cure for type 1 diabetes after all. Read on to get all the details.

Is it possible to reverse type 1 diabetes?
A recent study has shown that the drug streptozotocin when combined with a fasting mimicking diet may help reduce type 1 diabetes. iStock.com/RyanKing999

While type 2 diabetes is known to be reversible with diet and lifestyle changes, type 1 diabetes has long been thought to be a permanent condition that requires lifelong insulin dependence. Excitingly, a new study published just last month (1) suggests that a “fasting mimicking diet” could effectively reverse the pathology of type 1 diabetes in mice. While the potential for translating these findings to humans is still unclear, this is such a pivotal study that I wanted to take the time to unpack it piece by piece. First though, a bit of background to set the stage.

What Is a Fasting Mimicking Diet, Anyway?

We know that water-only fasting provides many health benefits, including reduced blood glucose, regeneration of the immune system, and cellular maintenance (2). But prolonged fasting is difficult for most people and can cause adverse effects on physical and mental health due to its extreme nature. Researchers have therefore been attempting to design diets that mimic the physiological benefits of prolonged fasting without the burden of complete food restriction.

Fasting mimicking diet may reverse type 1 diabetes

This type of diet is called a fasting mimicking diet (FMD). It is a very-low-calorie, low-protein, high-fat diet that causes changes in glucose, ketone bodies, and specific growth factors similar to those seen during prolonged water-only fasting. The FMD is characterized by cycles of caloric restriction and refeeding. For example, in mouse models of FMD, researchers restrict the amount of food the mouse has access to for four days, followed by three days of unrestricted feeding every week. In humans, one FMD cycle consists of five days of restriction, and eating resumes as usual for the rest of the month. This is typically repeated for three months (3).

Soon, we’ll jump into the results of the study to look at the intriguing effects of an FMD. But first, let’s briefly review what happens to the body in type 1 diabetes.

Pancreatic Anatomy and Type 1 Diabetes

The pancreas contains regions called islets, which are dense clusters of cells that are responsible for secreting hormones. The two main types of endocrine cells are insulin-producing β cells and glucagon-producing α cells. Pancreatic β cells are among the most sensitive cells to nutrient status.

When you eat a meal, they release insulin, which helps to shuttle glucose from the bloodstream into cells to be used for energy production. Between meals, glucagon helps to maintain a minimum level of glucose in circulation.

Type 1 diabetes is an autoimmune condition in which the body’s own immune system attacks and destroys the insulin-producing β cells of the pancreas. It is widely accepted that β cells in the adult pancreas replicate at an extremely low rate (4, 5), and that new β cell formation occurs very rarely (6). The β cell depletion and resulting loss of insulin secretion characteristic of type 1 diabetes is therefore thought to be irreversible.

Exciting developments in stem cell therapy may have potential for treating type 1 diabetes, but this invasive procedure would require complete removal of the dysfunctional pancreas, stem cell transplant, and activation of a complex genetic program to generate a new one. Enter the fasting mimicking diet.

The Results Are In: FMD Reverses Type 1 Diabetes in Mice

I know this is the part you’re all waiting for, so let’s get right to it. The researchers used a mouse model of type 1 diabetes, in which scientists use high doses of the drug streptozotocin (STZ) to cause depletion of β cells (7). Just five days of treatment with STZ was enough to elevate blood glucose, at which point the researchers started half of the mice on their first FMD cycle. The other half of the mice were left to eat unrestricted.

FMD restores insulin-dependent glucose control
In STZ-treated mice eating as much chow as they pleased, blood glucose levels continued to skyrocket. In contrast, mice receiving regular FMD cycles had blood glucose and insulin levels that returned to nearly normal levels by around day 50. Furthermore, glucose tolerance tests at this time point confirmed that FMD cycles in mice improved the ability to clear excess glucose from the blood.

FMD improves the cytokine profile
They decided to measure other substances in the blood as well. Analyzing immune signaling molecules called cytokines can tell us a lot about how the immune system is interfacing with the rest of the body. In this study, they found that mice on regular FMD cycles had reduced cytokines associated with inflammation and β cell damage (TNFα, IL-12) and increased levels of anti-inflammatory cytokines associated with β cell regeneration (IL-2, IL-10).

FMD triggers the regeneration of pancreatic beta cells
All this is great, but what the researchers really wanted to know was if the improvement in blood glucose control and changes in cytokines was mirrored by functional changes in the pancreas. Using cell staining techniques, they found that STZ treatment resulted in a dramatic (85 percent) decrease in the number of insulin-secreting β cells and an increase of non-hormone-producing cells. But with just a few FMD cycles of caloric restriction and refeeding, many of these non-α/β cells redifferentiated into functional insulin-secreting β cells (1)!

Turning Back Time: Reawakening Embryonic Genes

How was the FMD doing this? The researchers were curious too and wondered if epigenetics were responsible. They ground up some of the pancreatic tissue from the mice and used RNA sequencing to determine which genes were being expressed.

They found that the FMD is able to turn back the clock, promoting a gene expression profile in adult mice that is usually only observed during embryonic and fetal development. This is quite an astonishing finding.

I’ve covered epigenetics before—the idea that expression of certain genes can be turned on or off, depending on what stimuli are present. Essentially, the genetic blueprint for building a pancreas is present in every single cell in the body, from the womb through adulthood, as is the blueprint for every organ and structure of your body. But this genetic blueprint only gets turned on at certain times and in certain cells, when the proper signals are present.

For example, in normal mouse development, pancreatic progenitor cells express the proteins Sox17 and Pdx1 around embryonic day 8.5. Some of these pancreatic progenitors are converted into endocrine precursor cells, which then express the protein Ngn3 from embryonic day 11.5 to 18. These Ngn3-expressing precursors ultimately give rise to all of the islet endocrine cells. These proteins are usually not expressed at all once a mouse reaches adulthood.

However, the results of this study suggest that an FMD can induce expression of these embryonic development and β cell reprogramming markers. When the researchers performed the experiments again but intentionally destroyed the Ngn3 cell lineage, they found that FMD-induced β cell regeneration did not occur. This suggests that epigenetic reprogramming is responsible for the improved glucose tolerance and islet regeneration (1).

Beyond Mice: Regeneration in the Human Pancreas

Okay, so FMD reverses type 1 diabetes in mice. But what about humans? Unfortunately, it’s pretty hard to measure the regeneration of a pancreas in living humans, since we can’t collect human tissue like we can mouse tissue. So instead, the researchers performed ex vivo (outside the body) experiments on cultured human pancreatic islets from both healthy people and type 1 diabetics.

Ingeniously, they separately enrolled five human subjects in an FMD lasting five days and took blood samples at baseline and at day five of the FMD. The post-FMD blood serum samples had higher levels of growth factors and ketone bodies and lower levels of glucose, as expected. The researchers then took the cultured pancreatic islets and bathed them in the collected samples. In both healthy islets and type 1 diabetic islets exposed to the FMD-treated serum, there was a trend toward glucose-dependent induction of embryonic genes Sox2 and Ngn3.

They then tried applying commercially available “fasting mimicking” culture mediums that were low in glucose and serum to the cultured islets. When supplied with just this small amount of glucose, insulin secretion was stimulated in both healthy and diabetic islets. There were also major changes in β cell reprogramming markers (1).

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Were We Meant to Eat Three Times a Day?

I’ve written before about the mismatch hypothesis—the idea that our genes have not caught up to our modern lifestyle. Our hunter–gatherer ancestors probably had periodic variation of food scarcity and hunting success and likely rarely ate three times a day. The ability of animals to deal with food deprivation is an adaptive response that is conserved across species. In times of scarcity, a mild atrophy of tissues and organs minimizes energy expenditure. Upon refeeding, the body can build these tissues back up to their normal volume (8).

This raises a few interesting questions: is expression of these “embryonic” genes in adulthood really abnormal? Or is it possible that we are meant to have transient expression of these “embryonic” genes periodically throughout our lifetime?  Could our constantly fed state in most of the Western world be the true “abnormal” gene expression pattern? I certainly hope to see more research in this area, especially in humans.

Answers to Your Burning Questions

What’s the takeaway?
In a mouse model of Type 1 diabetes, a fasting mimicking diet causes a short-term reduction in β cell number, which returns to normal levels after refeeding. This occurs through lineage reprogramming and β cell regeneration, effectively restoring insulin production! Similar changes were seen in a cultured human pancreas, but more research is necessary to confirm that β cell regeneration also occurs in living humans.

What about type 2 diabetes? Since I’ve written before about reversing type 2 diabetes with diet, I decided to focus this article on type 1 diabetes. But the research I unpacked in this article was actually only half of the findings from this influential study. The other half of the experiments used a type 2 diabetes mouse model and showed that FMD was also able to rescue mice from late-stage type 2 diabetes. β cell number and insulin secretion were restored after six to eight cycles of FMD and refeeding (1).

Where can I try an FMD? The FMD, as studied in clinical trials, is currently available from Prolon as a specific package of prepared foods and micronutrients. It is intended to be administered under a doctor’s supervision. It’s very likely that a “homemade” version with a similar number of calories and similar composition of carbohydrate, fat, and protein would have the same effects, but this hasn’t yet been studied in a clinical trial. As I’ve written before, fasting is not right for everyone, so please consult with a healthcare practitioner before trying this at home.

Is it really as simple as an FMD? Maybe, but probably not. If in fact this research translates to humans, an FMD may regenerate your pancreas and restore insulin production in the short term, but it’s not going to stop your immune system from destroying it again. You would still need to address the root cause of disease, which is most likely an underlying food intolerance producing antibodies that are cross-reacting with islet cells. I would surmise that an FMD combined with the Paleo autoimmune protocol might just do the trick, but this remains to be tested.

Where can I dive deeper into the scientific research? Head over to the Kresser Institute blog, where I take an even closer look at the latest medical research. Be sure to check out my recent blog post on the benefits of FMDs for cancer, aging, metabolic disease, cognitive health, and more.

We certainly don’t have all the answers yet. Stay tuned for more discussion on my blog about the benefits of fasting mimicking diets and how to apply them in your life. This is certainly a fascinating topic and one that I’ll continue to cover in future blogs and podcasts as we learn more.

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Join the conversation

  1. I found about those studies a few months ago and as a type 1 diabetic having already tried a bunch of things (including switching to low-carb/paleo for easier blood sugar management), I decided to try a fasting experiment. Since I didn’t have a lot of guidance to go with, I went with a 4-5 days fasting followed by 25 days of normal eating.

    I did 3 full cycles before getting tested again for C-peptides (and other markers) but nothing significant showed up. I still think that fasting had a few nice benefits like helping me fine-tune my basal insulin as well as providing me with an easy way to get an almost flat blood sugar during fasting (which resulted in an a1c of 4.8).

    I’d like to try again especially after reading this but it would be nice to get more guidance as far as potential tests that could be done to indicate progress (or lack thereof) as well as the best protocol to follow.

    I did write down notes as I was fasting about how I was feeling and I also collected ketone levels (which I was testing 4 times a day with the Precision Xtra) and I have my continuous glucose monitor data as well. I’m not sharing my notes/data publicly but I’d be open to sharing to someone who would have something useful to do with it.

    • Hi Alex – did you suspend giving yourself exogenous insulin during your 4-5 days of fasting?

      • I’m normally on humalog / levemir and I did stop humalog for the duration of the fasts. My levemir was reduced to 1.25 units (3 times a day, as before) in order to keep my blood sugar to normal levels.

        The idea wasn’t that I’d stop needing basal insulin during fasts but that maybe I’d eventually see benefits like the studies have been suggestion could happen.

    • Just because I often didn’t have enough time to eat during my post-graduate studies and not for any medical reasons, I used to skip eating for up to four days at a time. I noticed absolutely no change in insulin dose or the way I felt after returning to a normal eating pattern. In general, no dietary or lifestyle interventions can be expected to ameliorate type 1 diabetes, since the beta cells of the pancreas which have been destroyed by the initial autoimmune attack cannot regenerate to any clinically significant extent.

      • I’m surprised about your statement. That must mean that your basal rate was absolutely perfect before you went in those fasts. I assume that because you weren’t eating, you also skipped bolus insulin?

        I’m also a bit skeptical of your certainty about the non-reversal of type 1. If there’s something I’ve learned in the last few years, it’s that it’s always healthy to remain open to new discoveries that might alter our understanding.

        • While fasting, I omitted the rapid-acting insulin normally taken at meals, and I also greatly reduced the background insulin, Lantus, which I normally took. I checked blood sugar levels often during this period, and maintained a fairly normal blood sugar level. The only limit I found to the amount of time I could fast was with my energy levels, which got too low to work by the end of the fourth day.

    • Good for you. 10th day fasting with an insulin pump. Watching this study but I think they are focusing on the wrong thing. But…this fast is working!!!! Like you, I’m keeping a diary. 34 years on a pump and feeling great. Had to do the fast because I’m allergic to all insulins not the preservatives. There are 1/2 of 1% of us in the world. Fasting allows me to decrease my insulin to a level that doesn’t trigger an allergic response.

  2. Indian traditional system of medicine, Ayurveda, explains very effective treatment for Diabetes, and its completely natural and side-effect free. Refer: https://www.superbeing.in/diabetes-ayurvedic-treatment/. Why is such treatment systems which existed for more than 5000 years, just couldn’t reach the popularity. Because the consequences of chemical medication is always huge.

  3. I have always been told the production of keytones was dangerous for the body. I would like to try FMD. Could someone advise me on the above, as I thought fasting carries the risk of increased keys?

  4. I don’t think Type 1 diabetes is a metabolic disease. It has some genetic component plus triggering toxic load (viral, bacterial, heavy metals and dysbiosis also). I think this kind of diet could help with blood sugar regulation but cannot resolve the true cause of this disease.

    • Type 1 diabetes is an autoimmune disease, and I don’t believe it has genetic component, certainly viral and bacterial, heavy metals and gut disbiosis can cause autoimmune disease, but not genetic. I would look into vaccination as a possible cause of Type 1 diabetes.

      • Vaccination brings more toxic load to the body so definitely a huge factor in Type 1 diabetes. Especially Rotavirus vaccine is shown to cause it. However I believe some people are more prone to autoimmune diseases consitituitionally, like people having MTHFR mutations whose detoxification pathways do not work well.

      • I also don’t believe the genetic component. I am Type 1 Diabetic and there is absolutely no history of it in my family at all.

  5. This is a really interesting article, thanks for sharing. My husband has type 1 diabetes. He got it as an adult. I’m pretty sure he has some functioning beta cells left because every once in a while for no discernable reason his glucose levels drop lower than expected. I would just caution anyone with type 1 who is thinking of experimenting with this diet to keep this in mind. If your body starts regenerating beta cells you could have sudden glucose drops leading to seizures. Obviously even more frequent glucose testing than usual would be needed.

    I hope there will be more human trials in the future. This has such important implications for all kinds of things. Thanks for keeping us updated, Chris!

    • That’s because Type 1 diabetes is an autoimmune disease. I would check for gut dysbiosis and heavy metal toxicity. And work on those.

  6. I have had Type I Diabetes for almost 34 years. I was diagnosed with an ulcer (H pilori as it is now called) 2 years prior to the Diabetes diagnosis. I treated the ulcer with Tagamet, which was only available by prescription then. After the ground breaking discovery about the real causes of ulcers (it’s a friggen bacteria!), I wonder if this H Pilori is the real culprit behind my Type I Diabetes. I just discovered last month that I still have that damned H Pilori germ still in me. Maybe that led to Diabetes Type I. I need to get rid of the H Pilori, but don’t want to take antibiotics. I also want to do this fasting exercise. Yikes!

    • David, in his book Herbal Antibiotics, Stephen Buhner has much advice on treating H. pylori with herbs. Buhner’s books are really good. They helped me to treat a very serious case of Lyme which was only getting worse after trying everything under the care of a Lyme literate doctor. The iv antibiotics i used to treat the Lyme about killed me. The herbal treatment has many side effects, all of which are beneficial.

    • I would consult a good herbalist for your H.Pylori issue. There are many great herbal medicine that can deal with this naturally without the use of antibiotic.

  7. Research results from mice literally never translate into meaningful results for type 1 diabetics, so I am not much impressed by mice experiments. Also, given the extremely low c-peptide values in nearly all type 1 patients you can find today, there must be so few beta cells left that there is nothing present to regenerate, even under the best of conditions. Only if you could intervene in patients at the first moment they were becoming type 1 patients could this method have any chance of working. Type 1 diabetes is also clearly a pathological state, given its very small incidence and genetic component, so there is nothing about it suggestive of the way people were originally designed to eat. If type 1 diabetes were a normal response to the new diet of civilization, everyone would have It, instead of just one in 300.

  8. Fascinating study, and so much more insightful when analyzed through the lens of ancestral health. Very cool to see how Chris is able to make sense of these findings (or at least pose a very plausible explanation) by simply using evolutionary logic. We should take a hard look at our cultural norm of eating three times a day, and think about why and if we should be doing that!

  9. Love all the articles you write on type 1 diabetes. I have LADA and follow a paleo diet. Still have off the charts autoantibodies but well controlled Hba1c. Definitely see the point in exploring underlying cause which I am about to do and I believe food intolerances are a big issue. Would definitely try fasting. Any special advice though for a female with very low ferratin levels? I am minded to try to address the ferratin levels first before trying fasting

    • Your situation sounds similar to mine. I haven’t yet met anyone who has LADA. I’ve controlled it by a mostly paleo diet for abou 7 years now. I can get the A1Cs to the 5.6 to 6.1 range (usually around 5.9). The GAD antibodies are 150-200 however, and I definitely can’t eat high or even medium glycemic food. Would be interested in being in touch to see how you manage it.

      • Hey Jane, I too haven’t met anyone else with LADA but am told there’s lots of us out there.

        I follow a paleo diet. I was AIP but have reintroduced foods. I carefully watched arch my carbs like you.

        I’d be happy to stay in touch. I’m based in NZ where are you?

      • I’m a LADA, for 6 years now, controlling with diet only, first went paleo but now have to be keto to keep BG in range. Have seen this study before, just a shame its only on mice. Wish they’d open up a study for humans, I’d be game!!

    • I’m a Lada too (6 years), need to be keto low carb to keep BG number in a healthy range, still not on insulin. Wish they would do a human trial, I’d be game!

  10. Well, it is incredible news but as always I see people reacting as if what you just said was proof that this study was evidence. It is not and it is disheartening to get people’s hopes up without telling them the entire story. The study was poorly done and on animals not humans. Recommendations do not jump species. Also, Type Is are not always born that way. Some are infected with a virus and recover. Some make a minimal amount of their own insulin and are not totally deficient. This needs much more study, replicability, controlled variables and ON HUMANS.

  11. I first heard about the fasting mimicking diet from the FoundMyFitness podcast: Dr. Rhonda Patrick interview of Dr. Valter Longo. It can be found on the podcast’s RSS feed here:
    Just search for “valter” using your browser to find the episode. It was posted September 30 2016. It is also on youtube:

    I’d like to see if somebody can come up with a real food meal plan that is similar to Prolon.

  12. Why doesn’t anyone eat pancreas anymore… imagine the fasting mimicking diet with 1 to 2 servings of pancreas per week.

    Pancreatic enzymes may help with food allergies by improving digestion. In order for a food molecule to produce an allergic response it must be a fairly large molecule. In studies performed in the 1930s and 1940s, pancreatic enzymes were shown to be quite effective in preventing food allergies. Typically individuals who do not secrete enough proteases will suffer from multiple food allergies.

    Many experts have long held the belief that glandular medicines exert a “tissue-sparing” effect on a person’s bodily tissues. This mechanism is by way of either neutralizing the auto-antibody attack on specific organ cells, or by way of supplying the right kinds of nutrients and enzymes highly specific, that allow the corresponding organ to rest up.

    Pancreatic glandular not only benefits digestion and nutrient assimilation, but may also increase pancreatic reserves. Thereby resting the pancreas in day-to-day functioning.

    The best part is that you can find pasture-raised, grassfed and grass finished pancreas on the cheap… about $4 to $5 per pound.

  13. >>You would still need to address the root cause of disease, which is most likely an underlying food intolerance

    I would like to request a future article with more on how to find this food intolerance. Is trying the Paleo autoimmune protocol enough, or might food allergy testing also be helpful.

    • And that is the problem. Food intolerances are factors in Metabolism and when you’ve avoided a detailed understanding of the subject you tend to go look somewhere else. And this is why we have mess and have made so little progress in so many places.

    • An elimination diet and food journal of results is the best way to determine food sensitivites.

  14. Another pin goes down. What this implies is that Type 1 is not fundamentally a genetic disease but is a metabolic disease. Since the genetic dysfunction may be reversed by a change in metabolism this tells us which is the cause and which the effect. People tend to apply what they already know and genetics has been an in thing for some time while the academic subject of human metabolism is so complex it is generally avoided. Taking courses in human metabolism my be an easy way to hurt ones GPA.
    The Golden Retriever Club has been funding a research project looking for the genetic cause of the very high cancer rate in Goldens, about 70% but this week circulated current advice on how to reduce the chance for your dog. Interestingly each recommendation involved influence upon the metabolism. We have almost a condition of group denial just as we’ve had with the lipid hypothesis. Its the reason the Wars on Cancer, going back to the first one initiated by Richard Nixon, have failed. The incidence of cancer has risen consistently over the years with the exception of when we stopped medical treatment that was causing it; hormone replacement for example, again a metabolic intervention. However there have already been demonstrated cures in research treating it as a fundamentally metabolic disease which causes genetic damage. Yes indeed, drying the pavement doesn’t stop it raining.

  15. This is incredible news!! Thank you for sharing. I look forward to hear more about this protocol. Epigenetics is the future of health, we must study and learn how to turn those switches on and off.

    • And one of the most important ways we can turn those epigenetic switches on or off is by addressing and resolving our usual hypervigilant emotional state. A state of underlying anxiety about imagined futures brings new born cells into a hostile biochemical environment and makes immune cells in particular trigger happy. Remember, almost a million cells, most of them immune cells, are born every single second in our bodies! But the good news is that they don’t live very long, four days maximum. So by finding a way to lower your anxiety levels has almost immediate effects on your health.

      • I agree, stress is one of the most damaging if not THE most damaging aspect on our health. We live in fear base times and things are getting worst every day. Nature has lost its place in our lives, I think it is the only thing that can save us…

  16. Is this diet renamed, just because it uses low calories?
    Or because the general medical community is resistant to the term “ketogenic”?
    Otherwise, FMD seems like a ketogenic diet. Or a “low carb/high fat; or a high fat/low carb diet, for that matter. Why do people keep trying to reinvent the wheel [name of it]?
    Because, low calories can be applied to ANY dietary choices, pretty much…does that mean any diet that uses low calories, must be renamed?
    Isn’t it confusing for most public, to be faced with so many names for pretty much the same the same thing? If anything, it could be called “low-calorie ketogenic”, to make sure more people understand what it is from the name.

  17. I don’t buy the idea of “auto immune disease”, where the body decides to attack itself. If it indeed decides to attack itself, it is doing so for a reason. It is up to the boneheaded scientists to stop with their warfare metaphors (attack/fight/battle/annihilate) for disease and find out WHY the body does the things it does. Always, there is a legitimate reason. Our creator was not a fool.

    Our bodies don’t hate us, don’t attack us, don’t do battle with us, don’t betray us (as whining cancer patients like to claim). For everything there’s a reason. For every bad symptom we have, it’s so something even worse doesn’t happen. It’s up to us to figure it out.

    • You mean our bodies are foolproof? You mean there are no ways to trick the body into creating harm to itself?

    • Samia, the body does not ‘decide’ to attack itself, it is not a matter of willful choice as you imply, and auto immune diseases are not an ‘idea’ to be bought into. Acquaint yourself with medical science, it’s not necessarily an anathema to your creator

    • You might find this interesting : http://www.veroniquemead.com/dm1.php

      “According to a model that seeks to understand the intelligence behind physiological activities, it is hypothesized that the immune system is actively recruited by the nervous system in individuals who eventually develop type 1 diabetes. In these instances, the immune system destroys insulin producing cells because the nervous system is conditioned towards a state of sympathetic dominance, which promotes increases in glucose and simultaneous inhibition of insulin secretion and activity. “

      • Another theory growing in popularity is that there is some genetic defect in the form of the beta cells in people disposed to develop type 1 diabetes, and under the right stressors, the immune system recognizes this defect as a signal that the patient’s own beta cells are foreign tissue, and so attacks them.

        But why worry about reversing the attack after it has already destroyed the beta cells? Even if the autoimmune attack is entirely halted, the beta cells will never regrow to any clinically significant extent. It would be smarter to forget about getting into the weeds of manipulating the immune system, and instead just concentrate on developing encapsulated islet cells which are shielded against both the immune and autoimmune response, and which could functionally cure type 1 diabetes.