This year’s virtual European Association for the Study of Diabetes (EASD) conference brought together thousands of researchers to share their latest discoveries and knowledge.
Previously, we shared EASD highlights on the latest research that will help people with diabetes live better and more confident lives, prevent type 2 diabetes and improve diabetes care.
Here, we’re covering developments towards treatments to cure or prevent type 1 and type 2 diabetes.
Beyond insulin
We’re fast approaching 100 years since the discovery of insulin. It was one of the most monumental medical breakthroughs in history and at the time was hailed as a cure for type 1 diabetes.
One hundred years later, insulin is still the only treatment we have for type 1 diabetes and our idea of a cure has changed. Scientists are striving for the next leap forward that could replace insulin therapy and Dr Alexandra Smink updated us on one potential route.
Islet transplants, where clusters of cells (called islets) taken from donor pancreases are transplanted into people with type 1 diabetes, already exist. But the donated cells stop working over time and people remain reliant on insulin injections or pumps.
Dr Smink is trying to find a better way of transplanting islets so that we can help people with type 1 diabetes make enough of their own insulin again. She has created a transplantation device that replacement pancreas cells sit inside. It acts as an ideal home for islets, protecting them from damage and helping them to produce insulin for longer.
Dr Smirk described how, just like our ideal home, a transplantation device needs:
an oxygen and food supply: her device allows blood vessels to grow inside it and so that they can supply the islets with the things they need to survive. Islets make up just 2% of the pancreas, but demand 20% of the pancreas’ blood supply. That's why this vascularisation is vital.
communication with the outside world: we need to make sure transplanted cells can ‘talk’ to the rest of the body and sense changes in blood glucose (sugar) levels. Dr Smirk has recreated a support structure that surrounds islets in the pancreas, called an extracellular matrix. It should boost communication and improve how well transplanted cells work.
- a security system to protect from attackers: in this case, transplanted cells need protection from the immune system. The device needs to block lurking immune cells from getting in and destroying the insulin-producing cells that sit inside.
Dr Smirk has been testing this innovative device in mice, using different doses of islets to find out what works best. She found that blood sugar levels in mice with diabetes who received a transplant of 800 or 1,200 islets returned to a healthy level. When the device is removed sugar levels immediately rise again.
But Dr Smirk explained there were still room for home improvements as there was still some damage to cells, they needed a high number of donor islets to see any benefit and it took a long time for blood sugar levels to return to a healthy level and stay stable (around 45 days). There’s more research to be done, but it’s an exciting area that we’ll be keeping a close eye on.
Getting to the gut of the matter
Our gut is home to millions of bacteria and other microorganisms, known as our gut microbiome. It can influence our health in different ways and research has pointed to potential a link between the makeup of our gut microbiome and risk of both type 1 and type 2 diabetes.
We don’t yet fully understand the direction of this relationship: does our gut bacteria play a role in the development of diabetes? Does living with diabetes cause changes to our microbiome? Or is it both? But we do know that we can alter our gut microbiome. This opens up the possibility of targeting the gut as a way to help prevent or slow diabetes.
To test this theory further, scientists have turned to poo. Research into Faecal Microbiota Transplants (FMT) has boomed in recent years and there are now about 300 trials underway looking at the potential of faeces to treat a range of health conditions, including obesity, non-alcoholic fatty liver disease, and type 1 and type 2 diabetes. FMT involves infusing stool from a healthy person into the colon of another person to help boost their diversity and number of ‘friendly’ gut bacteria.
Professor Max Nieuwdorp is a leading researcher in this field. He’s found that people with type 2 diabetes who receive donor faeces from people of a healthy weight show an increase in insulin sensitivity of between 20-50%, compared to people with type 2 who received their own faeces. People with high insulin sensitivity are better able to use the insulin they produce and therefore this could help to improve their blood sugar levels.
Professor Nieuwdorp and his team have also been exploring the potential of FMT to protect surviving insulin-producing beta cells in people newly diagnosed with type 1 diabetes. The more beta cells we can protect, the more insulin you can produce on your own.
In a recent trial, 20 people with type 1 were given healthy donor stool and 20 were given their own stool. Everyone received three transplants over six months and the researchers studied how much of their own insulin participants were making.
Surprisingly, they found that the group who received their own faeces back retained more of their insulin-producing capacity and saw longer ‘honeymoon periods’. Whereas FMT from a healthy donor didn’t help to preserve insulin production as much, although Professor Nieuwdorp noted it did seem to help more than no transplant at all.
He concluded that, yes, there are ways of manipulating gut microbiota in order to change the course of type 1 or type 2, but it’s not a clear-cut story. It likely depends on what’s in the stool that’s being transplanted. And there are studies happening right now that are building on FMT by trying to isolate specific bacteria from faeces and just give people the ones they’re missing.
As we learn more about the role gut microbiota plays in the development of type 1 and type 2 diabetes, we could home in on culpable bacteria and, in the future, develop treatments that target these to prevent or slow the conditions.
