New research identifying the untapped potential of a molecule secreted by frogs to treat type 2 diabetes is one of the innovations that has been presented at our professional conference (DUKPC).
It’s that time of year again, when thousands of diabetes researchers and healthcare professionals gather at our professional conference (DUKPC). There’s a jam-packed itinerary of lectures, training sessions and networking, with plenty of exciting updates on the latest in diabetes research.
Today at DUKPC we heard about innovations edging us closer to new diabetes treatments:
A molecule produced by frog skin could boost insulin production in type 2 diabetes
Progress towards understanding someone’s chances of type 2 diabetes remission
Studies exploring new treatments to combat hypos in type 1 diabetes
Could frogs spawn a new treatment for type 2?
Although there are a range of different medication options to treat type 2 diabetes, for many people managing blood sugar levels can be a real challenge. So, researchers have turned to innovative sources in the search for more effective treatments.
One family of type 2 medications, called GLP-1 agonists, have been inspired by molecules found in animal venom. And previous research we funded found that a molecule found in skin secretions from the East Asian bullfrog can also boot insulin release and suppress glucagon, a hormone that raises blood sugars.
At DUKPC, Dr Opeolu Ojo at the University of Wolverhampton presented findings from his latest study. He explored what happens when a lab-made version of the frog skin molecule (called tigerinin-1) is combined with a hormone called GIP. GIP is a component of an existing type 2 diabetes drug, tirzepatide (Mounjaro).
The team found that when combined, the two molecules didn’t cause any safety concerns. They then discovered that in mice with type 2 diabetes, the combination treatment increased the amount of insulin made by 50% compared to the frog molecule alone, and by 30% when only using GIP.
The combination drug was also more effective at improving glucose tolerance – a measure of how well the body moves glucose out of the blood and into cells in mice, than the frog molecule or GIP alone.
Dr Opeolu Ojo said:
“Our research has uncovered great potentials of peptides from amphibian skin secretions as novel agents for treating type 2 diabetes. By combining these peptides with some of the molecules that our body produces naturally, our desire is to create a safe and powerful alternative to current anti-diabetic medications which have many challenges, including their side effects and the ability to restore the body’s ability to control blood glucose.”
This research is still at an early stage, but we look forward to more studies, which will be needed to determine if the treatment would be safe or effective in people with type 2 diabetes.
The ins and outs of type 2 remission
Today at DUKPC, our DiRECT researchers revealed their latest findings, showing weight loss can help some people go into type 2 diabetes remission and stay there for at least five years. You can read more about what they found here.
But the DiRECT results also highlight that this doesn’t work for everyone.
We’ve been funding other remission research to help us pin down what determines if someone can go into remission. We know that the longer people have been living with type 2 diabetes for, the harder remission can be. Scientists think this is because their beta cells have reached a point of no return and aren’t able to recover.
But as we can’t access the beta cells of a living person to check their status, it’s difficult to know someone’s chance of going into remission. Or to study precisely what happens to beta cells when type 2 diabetes is put into remission.
With our funding, Dr Timothy Pullen at King’s College London has been looking for a solution. At DUKPC, he shared a blueprint of a new way scientists can study remission in the lab.
Dr Pullen’s method involves putting mice who have lived with type 2 diabetes for different lengths of time on a diet to trigger weight loss. He’s then devised a way to study the beta cells of mice that did and didn’t go into remission.
In future research, scientists can apply these methods to closely delve into how type 2 diabetes remission works and the key differences inside the pancreas when remission is and isn’t possible.
This will help us better understand how and why the length of time someone has lived with type 2 diabetes effects their chances of remission. And knowing this will be key to finding alternative routes to remission for people who can’t get there through weight loss.
Help for hypos in type 1 diabetes
Aiding alpha cells
At the moment we don’t have any treatments that work to help prevent hypos in people with type 1 diabetes. But scientists at DUKPC are trying to change that.
In type 1 diabetes, insulin-making beta cells in the pancreas are destroyed by the body’s own immune system. But they aren’t the only type of cells found in the pancreas. Alpha cells release a hormone called glucagon, which causes blood sugar levels to rise. Normally they should kick into action when blood sugar levels start to fall.
But there’s evidence that alpha cells can also fall victim of the immune system’s attack and seem to fail in some people with type 1 diabetes. This increases their risk of hypos (low blood sugar levels).
At DUKPC, researchers at the University of Oxford shared how they’re searching for ways to help alpha cells work better.
They’ve been investigating if a new treatment, called a somatostatin receptor-2 (SSTR2) antagonist, could help to boost the release of glucagon from alpha cells in response to low blood sugars in mice with type 1 diabetes. It works by blocking a hormone which prevents alpha cells from doing their job.
Researchers compared the amount of glucagon mice were producing with and without the treatment. Promisingly, they found the SSTR2 antagonist helped to restore the mice’s ability to produce glucagon when blood sugar levels dropped.
These are early findings and there’s more research needed. But this study shows the potential of SSTR2 antagonists to help reduce the risk of hypos in people with type 1 diabetes.
Metformin in type 1
Hypos happen when people with type 1 have too much insulin in their body. Some people with type 1 diabetes can still make tiny amounts of insulin from their own pancreas, and this can reduce the amount of insulin they need to inject or pump less insulin. In turn, taking less insulin can help to reduce the risk of hypos.
So, a team at the University of Glasgow ran a study to see if metformin – a treatment often used to help people with type 2 diabetes to use their own insulin more effectively – could help people with type 1 in a similar way.
The researchers recruited people aged 40 or over who’d lived with type 1 for more than five years. They gave them either metformin tablets or a harmless dummy tablet, called a placebo. Over three years, the researchers measured how much insulin from their own pancreas participants were making, and how often they were having hypos.
The results, shared at DUKPC, found no difference in insulin production between participants taking metformin or a placebo. But the researchers did find that people who were making more of their own insulin tended to have fewer hypos.
While this study didn’t find any benefits of metformin to help prevent hypos, the findings suggest that more research into new treatments to help people with type 1 to keep hold of their own insulin, could be really important in reducing the burden of hypos.
Check back tomorrow for our research highlights from day 2 at DUKPC.
