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Gallstone drug could be used to fight type 1

JDRF researchers at Stanford University have used a commonly-available drug for gallstones to prevent the onset of type 1 diabetes in mice.

If the results can be translated to humans with the condition, the drug’s widespread use could speed the path to its adoption.

The Stanford team, led by Dr Nadine Nagy, discovered the drug’s potential when they tried to determine how type 1 develops in the pancreas. They found that people who had been recently diagnosed with the condition had high levels of a substance called hyaluronan around their insulin-producing beta cells – much higher than either people without type 1, or people who had had the condition for many years.

Hyaluronan usually accumulates near injuries, such as sprains, when they become inflamed, and inflammation is a key part of the destructive process in autoimmune conditions. This suggested to the researchers that hyaluronan could be involved in the development of type 1.

To test whether the high levels were actually a cause - or simply an effect - of the immune attack, the researchers used a drug, called hymecromone, that blocks the body’s production of hyaluronan.

When mice that are prone to developing diabetes were given hymecromone, they stayed free from diabetes for at least a year, while those that were not quickly saw their blood glucose levels rise. However, the drug had to be taken consistently – once stopped, the effects wore off and the mice developed type 1.

Despite this, the researchers are now working with the US Food and Drug Administration to develop a clinical trial of the drug for people with type 1.

Karen Addington, Chief Executive of JDRF, said: ‘Finding exciting new possibilities for existing drugs – known as repurposing – is a very smart approach as the drug’s safety is already established. We funded this study and we’re delighted it has shown promise. But it remains to be seen whether this success in mice can be replicated in people.’


Psoriasis drug could protect insulin-producing cells in type 1 diabetes

JDRF researchers in the US have found that alefacept, a psoriasis drug that targets the immune system, could help keep insulin-producing cells safe in people with type 1 diabetes.

The results come from a two-year clinical trial of the drug in people who were newly diagnosed with type 1. The same team previously reported encouraging results in 2013 but now, 15 months after the last dose of alefacept, people who were given the drug needed to take less insulin day-to-day, and had higher levels of a protein called C-peptide – a by-product of insulin production – in their blood, than people given a placebo.

This suggests they were making more of their own insulin than people who did not take alefacept, despite both groups having had type 1 for more than two years.

When the researchers compared the levels of immune cells between the two groups, people who had taken alefacept had higher levels of cells that regulate the immune system, and lower levels of cells that are known to attack the pancreas in type 1.

Taken together, it appears the drug helped keep insulin-producing cells healthy by altering the immune system, reducing its ability to attack.

Dr Gerald Nepom, director of the Immune Tolerance Network, which conducted the trial, is cautiously optimistic about the next stage of the research: ‘Achieving long-term benefit following a short course of therapy is a challenging goal.’

‘Detailed analysis of the immune cell types in the blood of those who responded to the treatment will help us identify the best way to improve this type of immune therapy for people with type 1 diabetes and potentially other autoimmune conditions.’

Conor McKeever, Research Communication Officer at JDRF in the UK, commented: ‘It’s always exciting to see research using an existing drug because if it works, the path to getting the drug to people with type 1 should be clearer and quicker. We’ll be watching with interest to see what results come out of the next stage of the study.’

The results were published in The Journal of Clinical Investigation.


Behind the headlines: a laser-powered blood glucose test?

You may have seen the news today about a device that could check a person’s blood glucose levels without the need for fingerprick testing. Instead, the device uses a low-powered laser to measure blood glucose levels through the skin.

At the moment, the device, which is being developed at the University of Leeds, is in the early stages of testing: it is currently the size of a shoe box and has only been tested in a trial of 12 people. However if the results from the prototype are promising – the Leeds team believes they are – a smaller, more portable version could be developed to undergo a further round of testing.

This may even take the form of a device that continuously monitors blood glucose, according to Professor Gin Jose, who led the study: ‘Currently, we are piloting a bench top version in our clinical investigations but aim to develop two types of devices for the market. One will be a finger-touch device similar to a computer mouse. The other will be a wearable version for continuous monitoring.’

Conor McKeever, Research Communication Officer at JDRF in the UK, commented: 'It's great that scientists are innovating with different techniques to make life easier for people living with type 1 - we’ll be watching with interest to see how the team turns this prototype into new devices.’

‘However, much larger clinical trials of these devices will be necessary before any regulatory agency will consider them equivalent to fingerprick testing.'


Combined treatment for type 1 diabetes could stop the immune system in its tracks

JDRF researchers in California and Italy have successfully used ‘gene therapy’ to reverse the immune attack behind type 1 diabetes in mice.

Mice that received the treatment not only kept their remaining insulin-producing beta cells, but also stabilised their blood glucose levels without external insulin.

The researchers, led by Professor Maria Grazia Roncarolo, developed the treatment by combining two kinds of therapy that have shown promise for treating autoimmune conditions in the past. The first, gene therapy, saw them transfer part of a gene involved in insulin production into liver cells. This spurred the mice’s immune systems into stopping any rogue immune cells that might try to kill off insulin-producing cells. As a result, no more of these rogue cells were able to infiltrate the pancreas, even up to 33 weeks after the therapy. In comparison, mice that did not receive gene therapy had lost 80% of their insulin-producing cells after 33 weeks.

However, this part of the treatment did not reduce the number of immune cells present – it only maintained it. To allow the mice to restore their blood glucose levels, the researchers then used a single dose of a drug that can kill off immune cells. After this, 75% of the mice had blood glucose levels that stayed low for many weeks without needing external insulin.

The drug, called a monoclonal antibody, is often used after organ transplants to stop the immune system rejecting the organ. But there are issues with using these drugs continuously, as the body needs its immune system to fight off illnesses. So the fact that the treatment only needed a single dose – thanks to the addition of the gene therapy – is very promising.

Rachel Connor, Head of Research Communication at JDRF in the UK, said: ‘Over the last few years our understanding of how the immune system works in health and in type 1 diabetes has grown enormously. This innovative study has come up with a novel way of helping the immune system bring the attack on insulin producing beta cells under control, and even reverse it.

‘Gene therapy treatments are beginning to be tested in people now, so despite a long research journey ahead, approaches like this one may one day be able to help people with type 1 diabetes.'

The research was published in the journal Science Translational Medicine.


Seasonal switch: Genes behind type 1 diabetes turn on and off across the year

JDRF researchers at the University of Cambridge have found evidence that our immune systems change with the seasons – a finding that suggests a seasonal link to type 1 diabetes.

Scientists have known for some time that diagnosis rates of various conditions, including cardiovascular disease and type 1 diabetes, vary with the seasons. However, this is the first time that researchers have shown that this may be down to seasonal changes in how our immune systems function.

The study, published today in the journal Nature Communications, shows that the activity of almost a quarter of our genes differs according to the time of year, with some more active in winter and others more active in summer. This seasonality affects our immune cells and the composition of our blood and fat tissue.

‘This is a really surprising – and serendipitous – discovery as it could change how we identify the effects of the genes behind type 1 diabetes,’ said Professor John Todd, Director of the JDRF/Wellcome Trust Diabetes and Inflammation Laboratory at the Cambridge Institute for Medical Research.

‘In some ways, it’s obvious – it helps explain why so many diseases, from heart disease to mental illness, are much worse in the winter months – but no one had appreciated the extent to which this actually occurred. The implications for how we treat conditions like type 1 diabetes, and even how we plan our research studies, could be profound.’

An international team, led by researchers from the JDRF/Wellcome Trust Diabetes and Inflammation Laboratory, examined blood samples from over 16,000 people living in both the northern and southern hemispheres, in countries including the UK, USA, Iceland, Australia and The Gambia.

They found that thousands of genes were either more or less active depending on what time of year the samples were taken. One gene known as ARNTL was particularly interesting as previous studies have found that this gene suppresses inflammation, the body’s response to infection. The gene was found to be less active in winter, suggesting levels of inflammation should be higher during those months. Inflammation is a risk factor for a range of diseases – including autoimmune conditions such as type 1 – so it may be that in winter, the 'threshold' at which these conditions could be triggered could be more easily reached in those at greatest risk. 

Karen Addington, Chief Executive of JDRF in the UK, said: ‘We have long known there are more diagnoses of type 1 diabetes in winter. This study begins to reveal why. It identifies a biological mechanism we didn’t previously know of, which leaves the body seasonally more prone to the autoimmune attack seen in type 1 diabetes.’

‘While we all love winter sun, flying south for the whole of each winter isn’t something anyone can practically recommend as a way of preventing type 1 diabetes. But this new insight does open new avenues of research that could help untangle the complex web of genetic and environmental factors behind a diagnosis.’

Image: Four Seasons from Wikimedia Commons user Bdk, used under a Creative Commons licence.


Researchers harness 'nothing to see here' protein to improve cell transplants

JDRF researchers have found a protein that can protect insulin-producing beta cells from the immune system, potentially paving the way for beta cell transplants that don’t require anti-rejection drugs.

Professor Mark Poznansky and his team at Massachusetts General Hospital had been studying the protein, known as CXCL12, for many years because of its role in the immune system. It has a repellent effect that drives immune cells away from the area where they are produced so that they can fight infection in the rest of the body.

The team then turned this effect on its head, using the protein to repel the immune cells from the beta cells they mistakenly try to attack in type 1 diabetes. When they encased beta cells in a gel coating that contained the protein, and implanted them into mice with type 1, the researchers found the mice produced their own insulin for at least 300 days. This was over 6 times longer than in mice where the cells’ gel coating did not contain any of the protein.

If the work continues to prove successful, it could be used alongside JDRF beta cell research (such as that announced by Professor Doug Melton in October last year), to generate large numbers of implantable, insulin-producing cells that are kept safe from the immune system. This concept, known as encapsulation, would offer people with type 1 the opportunity to regain their insulin-producing cells, eliminating the need for insulin injections and carb counting.

Commenting on the finding, Professor Poznansky said: ‘The encouraging picture painted by our studies to date has led us to the next step in our research. JDRF is now funding a 2-year pilot study to investigate whether this approach of including CXCL12 in the gel capsule will work when greater numbers of capsules are implanted into larger animals.’

He continued: ‘One of the most exciting aspects of CXCL12 is that, if the protein proves safe and effective, its applications could go beyond use in encapsulated cell therapies: it might also be useful in developing drugs to block the autoimmune attack on still-active beta cells in the early stage of the condition, slowing or ultimately preventing the progression to insulin dependency.’

The research was published in the American Journal of Transplantation.


Injection of millions: massive investment follows Dr Melton’s stunning stem cell research breakthrough for type 1 diabetes

You’d be forgiven for suspecting that things sometimes go a bit quiet after global headlines shout about a type 1 diabetes research breakthrough.

But JDRF’s Harvard hero Doug Melton, whose work turning stem cells into insulin-producing beta cells made worldwide news last October, has announced two massive new business collaborations designed to bring his research to fruition sooner.

The first, which has raised £30 million from several companies including Medtronic, will aim to develop beta cells that can be transplanted into the body.  In type 1 diabetes, the immune system destroys these insulin-producing beta cells, so a procedure that could give them back to people could mean an end to insulin injections and blood glucose testing. It’s why we, too, are funding Dr Melton as part of our encapsulation research.

The second collaboration, a partnership with pharmaceutical company AstraZeneca, will see researchers study the beta cells to learn more about their biology, giving us new insights into how type 1 diabetes develops. The cells will also be tested against many of the drugs developed by AstraZeneca, to see if any could be used to cure or even prevent the condition.

Until now, beta cell research in both of these fields had been hindered by a lack of donated pancreases, and by the more lengthy process normally used to grow the cells in the lab. Work by Melton, and by other JDRF-funded researchers such as Timothy Kieffer, should therefore help speed up the process of turning lab-based discoveries into treatments for people with type 1 diabetes.

Dr Clare McVicker, Director of Research Advocacy at JDRF in the UK, said: ‘A £30m investment is a huge stamp of approval for Dr Melton’s research. Business only backs scientific developments when it sees true potential – and this could change type 1 diabetes treatment globally.’

Read more about Dr Melton here.


Behind the headlines: 'more children showing early signs of diabetes complications'

The media is reporting that 'more children are showing early signs of serious diabetes complications.'

These headlines – clearly alarming for parents of children with type 1 diabetes – stem from today’s release of the National Paediatric Diabetes Audit.

The report actually shows that long-term blood glucose control among UK children with type 1 diabetes is improving, not worsening, and this fact behind the headlines is heartening. The increase in children showing early indications of future potential complications is instead due to the fact that increasing number of children are developing the condition. Individual children with the condition are not increasingly at risk.

Of further reassurance to families affected by type 1 diabetes is the fact (stated by the report itself) that early signs of eye, kidney and foot complications in children can be reversed by good control of blood glucose levels.

Sarah Johnson, Director of Policy and Communications at type 1 diabetes charity JDRF, admitted aspects of the report were concerning. She said: 'Although we’re pleased to see an increase in the number of children achieving in-range blood glucose control, we are alarmed by the numbers showing signs of complications at such a young age. Improvements in treatment and early interventions to prevent these complications need to be prioritised urgently by the NHS, and healthcare professionals must be given the help and resource they need to help their young patients manage a serious, life-long condition.'

Some of the media headlines also focused on a detail of the report that stated 'one in four children over the age of 12 who have type 1 diabetes are classed as obese.'

She added: 'We also need to remember that obesity is not a cause of type 1 diabetes. Children with type 1 diabetes have similar rates of obesity as children in the general population – they don’t live in a bubble and are subject to all of the influences and issues that affect their friends and classmates.  Absolutely weight is a factor in helping achieve good blood glucose control, but nothing these children did, or did not do, caused their immune system to attack their pancreas.'


Behind the headlines: The Daily Mail – fact or fail?

The Daily Mail this morning reported the results of a study from the Lancet under the headline ‘Women with type 1 diabetes are 40 per cent more likely early to die than men with the disease’.

Yet as many people rightly pointed out in the article comments, this headline is somewhat misleading. It could lead people to think that women with type 1 diabetes more often die much younger than men with the condition. This is not the case.

It’s well-known that, on average, women live longer than men. However, in people who have type 1, both men and women have similar lifespans. This means that the effect of type 1 diabetes on lifespan is more pronounced in women than in men ­– this is where the Mail’s 40 per cent statistic comes from. The effect on women is 40 per cent bigger than the effect on men, which amounts to both men and women living a similar amount of time.

The same is true for the other statistics – women tend have lower rates of cardiovascular disease and stroke than men, so if type 1 puts both genders at a similar level, then the effect of having the condition is much bigger for women. They are not, as the Mail suggests, 37 per cent more likely to die of a stroke than men; it is that the effect for women is 37 per cent greater.

In addition, the overall effect of type 1 diabetes upon mortality is getting less and less every year. Last month, we reported a study that showed that people with type 1 are living longer than ever before, and we are funding numerous projects such as AdDIT to combat the threat of complications.

Despite this, both the Mail article and the Lancet study highlight an important point – women with type 1 are being more strongly affected by the condition than men, and we need to address this discrepancy. Studies have found that women have slightly higher HbA1c levels over their lifetimes, and as long-term hyperglycaemia raises the risk of complications, this could contribute to the difference.

Better treatments to support glucose management – including smart insulins and the artificial pancreas – would go a long way towards reducing the impact of type 1 on everyone.

Sarah Johnson, Director of Policy and Communications at JDRF, said: ‘We know that research has shown young girls and women with the condition are more likely to have poorer blood glucose control than their male counterparts. Whatever the reasons are behind that, what’s certain is that every single early death linked to type 1 diabetes is unacceptable.’

She added: 'One day, the cure will be found. To get there, we need research to be better supported.'


Inhaled insulin launches in the US

Afrezza, the inhaled insulin developed by MannKind and licensed to pharmaceutical company Sanofi, has gone on sale in America this week. This means that American adults with type 1 or type 2 diabetes can now get Afrezza on prescription as a bolus insulin.

However, the drug is not yet approved for people outside the US, for children or for people with chronic lung conditions.

Afrezza is taken using a thumb-sized inhaler at the start of the meal, and passes through the lungs into the bloodstream. The peak insulin level in the blood occurs around 12-15 minutes after use, making it more similar to insulin produced naturally by the pancreas in people without type 1. Most ‘rapid’ insulins peak 30-90 minutes after use.

This led JDRF to fund a trial using Afrezza in 2010, as part of a programme developing faster insulins for the artificial pancreas. The participants used it at meals to fine tune their blood glucose levels, alongside the slower-acting insulin being given by the artificial pancreas. This led to smaller blood glucose level peaks at mealtimes.

An additional benefit of the drug is that it could be used as by people who do not want to inject insulin. Pierre Chancel, Senior Vice President of Sanofi’s Diabetes Division, commented: ‘There is a recognized need for an insulin that doesn't require an injection, and our organization is committed to making this new treatment option available to patients.’

We previously covered Afrezza in June 2014 when it was approved for sale by the FDA, making it the only inhaled insulin on the market. A previous inhaled insulin developed by Pfizer, called Exubera, was withdrawn after poor sales and suggestions of an increased risk of lung cancer.


Behind the headlines: a probiotic cure for diabetes?

This morning, the Daily Express ran a headline saying ‘Breakthrough pill can CURE diabetes: New drug fights both types of killer disease’. So is it true, can a pill now cure both type 1 and type 2 diabetes?

Sadly, no. But the study behind the headline is really interesting.

Researchers at Cornell University, led by Professor John March, have developed a ‘probiotic’ pill containing modified bacteria that are typically found in the human gut and given them to rats with diabetes.

Central to the story is a hormone called glucagon-like peptide 1, better known as GLP-1. GLP-1 helps to regulate the body’s response to glucose in a meal. It does this by blocking the production of glucagon, so that glucagon does not act to raise glucose levels in the blood still further.

Professor March’s team engineered bacteria so that they would produce GLP-1, then gave a group of diabetic rats feed supplemented with this new ‘probiotic’ and compared them with a group of diabetic rats with un-supplemented feed. Rats given the supplemented feed developed insulin producing cells in their gut – some of the regular gut cells were ‘reprogrammed’ to make insulin. This meant that they showed significant increases in their insulin levels and the research teams estimated that these cells were sufficient to produce up to 33 per cent of a healthy rat’s insulin capacity.

So while this study does not herald a cure for type 1 diabetes, it does show that GLP-1 may have an important role to play in improving treatment for people with the condition.

GLP-1, and molecules that mimic its effect (known as GLP-1 agonists), have been widely researched in type 2 diabetes, and there are now a number of GLP-1 agonists available to help in treating type 2 diabetes. But these drugs have only recently started being investigated in type 1 diabetes – thanks in part to funding from JDRF.

Rachel Connor, Head of Research Communication at JDRF comments: ‘The Cornell team’s study adds to our understanding of the role GLP-1 and also demonstrates a novel way of increasing GLP-1 levels in the body. It’ll be interesting to see whether the same effects can be observed in humans with diabetes.’


JDRF researchers discover cell behind type 1 diabetes

Researchers at London’s Royal Free Hospital have found the immune system cell responsible for triggering the destruction of insulin-producing cells in type 1 diabetes.

Their finding could lead to new treatments that target this triggering process, potentially offering a way to cure or even prevent the condition.

Type 1 occurs when the body’s own immune system, which is meant to fight off diseases, attacks the cells in the pancreas that make insulin. Previous research has found that T cells, part of the immune system, are behind the attack, but this is the first time researchers have identified the specific kind of T cell involved.

The London team, led by Professor Lucy Walker, studied T cells from people with and people without type 1. They found that samples from people with type 1 contained much higher levels of molecules associated with a kind of T cell known as a ‘follicular helper T cell’.

These cells have previously been implicated in other autoimmune conditions such as lupus, but this is the first time they have been identified as being behind the autoimmune attack in type 1.

“Knowing more about the type of T cell that causes type 1 is definitely good news for future treatments” said Professor Walker. “It provides us with a new way of thinking about the cells that are causing the problem, and may allow us to develop different ways of interfering with them.”

While the discovery offers potential for research into a cure for type 1, it could also support research into preventing the condition, explained Professor Walker: “Measuring the level of this specific type of T cell in the blood could turn out to be a way of assessing someone's risk of developing type 1 ­– this is an idea we'd like to explore in the future.”

The study was published in the Journal of Clinical Investigation.


People with type 1 diabetes living longer, healthier lives

JDRF-funded researchers at the University of Dundee have found that people with type 1 diabetes are living longer than ever before.

While previous estimates have suggested that type 1 can reduce life expectancy by 15-20 years, Professor Helen Colhoun and her colleagues found this gap had narrowed to 11 years for men and 13 years for women. The difference was even smaller for older adults, reaching single digits for people aged 50-54.

Overall, life expectancy for people with type 1 has improved tremendously in just the last 40 years. In 1975, the difference between people with and without type 1 was almost 30 years, shrinking to less than 20 years in the 1990s.

However, the study shows that there are still improvements to be made, which is why JDRF continues to fund research into complications. AdDIT, a trial being run at the University of Cambridge, aims to prevent young people from developing heart and kidney diseases – highlighted by the Scottish research as two of the biggest factors that reduce life expectancy.

Better treatments, too, have an important effect. While good blood glucose control is encouraged at all ages, a US study also released today found good glucose management early on after diagnosis can give people with type 1 longer, healthier lives. JDRF-funded research into glucose control treatments such as the artificial pancreas and smart insulin is designed to make this challenging job, much easier.

Both the Scottish and American studies were published in the Journal of the American Medical Association.


Winners announced of 2014 research photo competition

We asked our researchers to send in images that showed their research in action, for the chance to win a £500 travel bursary (£250 for the runners-up). Here are the winning entries, with explanations from the researchers themselves.

1st place

Georgios Ponirakis, Clinical Research Coordinator at The University of Manchester

The photos show our team using In Vivo Corneal Confocal Microscopy (IVCCM) to test for nerve damage caused by type 1 diabetes. Nerve damage is a common complication of diabetes, so a rapid, non-invasive, clinical assessment technique for its detection - such as IVCCM - is useful to predict and prevent further complications.

We hope that by screening for long-term complications early on, we can prevent them from developing.

2nd place

Dr Sarah Cross, Postdoctoral Research Scientist at the Nuffield Department of Surgical Sciences and Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), University of Oxford

In June 2014, the Oxford Centre for Diabetes, Endocrinology and Metabolism held its first public engagement event, entitled 'Unravelling the Mysteries of Diabetes'. Our aim was to create fun and interactive ways to explain, to both adults and children, the diabetes research that is carried out in our centre, in order to make our research more accessible to the general public.

This photograph was taken during one of the guided tours of the DRWF Human Islet Isolation Facility, in which we demonstrated how we collect the parts of the pancreas that make insulin, the islets of Langerhans, from a donated organ in our clean room labs. These tours proved extremely popular with the public, who were able to discover both the long history of islet transplantation research in Oxford and how it is now translated to the clinic to combat hypo unawareness and allow insulin independence in patients with severe type 1 diabetes.

3rd place

Dr Sarah Cross, Postdoctoral Research Scientist at the Nuffield Department of Surgical Sciences and Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), University of Oxford

Islet transplantation is a classic example of recent research in type 1 diabetes that has enabled a novel treatment to be translated from 'bench to bedside'.

This series of photographs illustrates the process of human islets being extracted from a donor pancreas, infused into the recipient’s liver, and the transformation of a patient’s life from life-threatening hypo unawareness to stable blood glucose levels (and, in this patient, prolonged insulin independence). The microscopy image demonstrates the complex structure of the pancreas and the ongoing challenges of islet isolation. This challenge forms a central component of our JDRF-funded research.


Could a blood pressure drug help beta cells survive? People with type 1 diabetes will soon help researchers find out

A new clinical trial is due to begin shortly, testing whether a commonly used blood pressure drug, verapamil, can help remaining insulin-producing beta cells survive in people newly diagnosed with type 1 diabetes.

The trial is the result of many years of laboratory research – much of it supported by JDRF – gaining insights into how beta cells work in people with diabetes. The research team, led by Dr Anath Shalev at the University of Alabama at Birmingham, have found that when a person develops diabetes and their blood glucose levels rise, their body starts overproducing a protein called TXNIP. Research has shown that an excess of TXNIP in beta cells triggers a process of cell death, which of course makes it even harder for the body to regulate blood glucose effectively.

The research team then started to search for drugs that could help reduce TXNIP in beta cells. And they found that verapamil, which is widely used in the treatment of high blood pressure, irregular heartbeat and migraine headaches, fitted the job description.

Working with mice with diabetes, the team found that the drug was very effective – not just halting beta cell decline, but actually restoring the mice’s ability to make their own insulin. The team have planned the new clinical trial to find out if the drug can have a similar effect in people with type 1.

There is no current treatment for diabetes that targets beta cell growth and development in this way, so if the results of this trial are positive, it might establish a completely new treatment paradigm for type 1 diabetes.

This trial will be a stepping stone to see if the approach can work. In the best case scenario, this trial would see beta cell mass completely restored in all the people taking the drug in the study. This is unlikely – but a more subtle effect would still be very beneficial explains Dr Shalev: 'We know from previous large clinical studies that even a small amount of the patient’s own remaining beta cell mass has major beneficial outcomes and reduces complications. That’s probably because even a little bit of our body’s own beta cells can respond much more adequately to very fine fluctuations in our blood sugar — much more than we can ever do with injections or even sophisticated insulin pumps.'

The announcement of this clinical trial goes to show how important detailed ‘basic science’ studies in the lab can be – a thorough understanding of beta cells biology is what has made this trial possible. JDRF is proud to have supported the lab science that has got us to this point, and to be providing the funds for the clinical trial that will test whether the approach can work in people.

Karen Addington, Chief Executive of JDRF in the UK commented 'Repurposing existing drugs to address the fundamental challenges of type 1 diabetes – in this case the loss of the beta cells which make insulin - is a smart approach. Years of work in the lab to understand how beta cells work has allowed scientists to identify a target and then search out existing drugs that act on it. This trial will now allow us to see if the positive findings in animals can translate into humans. We eagerly await the results.’


Breaking news: Encapsulated stem cells implanted in to person with type 1 diabetes for first time

JDRF partner company ViaCyte has announced the first successful implant of its islet encapsulation system into a person with type 1 diabetes. The person was taking part in a University of California-based trial to assess the safety of the system.

Type 1 diabetes arises when the body’s immune system attacks and destroys the insulin-producing cells of the pancreas, leaving a person with type 1 unable to manage their own blood glucose levels without external sources of insulin. ViaCyte’s system replaces these insulin-producing cells, and could therefore allow a person with type 1 to produce their own insulin automatically in response to changing glucose levels.

The device, called VC-01, contains thousands of immature cells derived from stem cells in a credit card-sized capsule. Once implanted inside the body, these cells mature into insulin-producing cells and are kept safe from the immune system. This protection sets the treatment apart from traditional transplantation, where the cells are left unprotected and are eventually destroyed once again by the immune system.

Because the system uses stem cells, it also has the potential to treat far more people than transplantation, which is hampered by a lack of organ donors. Indeed, just two weeks ago, Dr Doug Melton, who has also received JDRF funding, announced an efficient method of producing thousands of insulin-producing cells from small numbers of stem cells in the lab.

However, the University of California trial is just the first of many that will be needed to see if the treatment is a success. The primary goal of this first study is to evaluate the safety of the VC-01 device in people who have had type 1 for at least three years, not to make them insulin independent. Subsequent trials will be needed to see how effective the device is over a number of years.

‘I’m really excited that this encapsulation system is being tested in a person with type 1 diabetes,’ said Karen Addington, CEO of JDRF in the UK . ‘Islet encapsulation has huge potential to transform the lives of people with type 1 – which is why we’re proud to support this and many other encapsulation projects around the world.’

Dr. Paul Laikind, President and CEO of ViaCyte, said: ‘Treating the first patient with our stem cell-derived islet replacement product candidate is an exciting next step in our quest to transform the way patients with type 1 diabetes are impacted by the condition.  Moving from a promising idea to a new medicine is a long and challenging journey and we are grateful to JDRF, and all its supporters, for the tremendous and continued support they have provided.’


Dr. Melton – the Harvard hero behind today’s type 1 diabetes stem cell breakthrough – thanks JDRF

You’ve seen the news today. Harvard stem cell researchers have announced a ‘giant leap forward’ in the quest to find a truly effective treatment for type 1 diabetes. 

With human embryonic stem cells as a starting point, the scientists are for the first time able to produce – in massive quantities – human insulin-producing beta cells equivalent in almost every way to normally functioning beta cells. It’s not yet a cure. But it’s big news.

Now meet the man who led this breakthrough.

Dr. Doug Melton is Co-scientific Director of the Harvard Stem Cell Institute. When his then-infant son Sam was diagnosed with type 1 diabetes 23 years ago, he dedicated his career to finding a cure for the condition. His daughter, Emma, also lives with type 1 diabetes.

The 61-year-old Cambridge graduate has previously been listed among TIME magazine’s 100 most influential people in the world. Jose Oberholtzer, Associate Professor of Surgery, Endocrinology and Diabetes and Bioengineering at the University of Illinois said: “Doug Melton has put in a life-time of hard work in finding a way of generating human islet cells in vitro. He made it.”

When he told his son and daughter about his breakthrough, they were surprisingly calm. He said: “I think like all kids, they always assumed that if I said I’d do this, I’d do it.”

Melton is now beginning a US$4 million project with JDRF, for the next stage of development of these cells. Expressing gratitude to the charity and its supporters, Dr. Melton said: “their support has been, and continues to be essential.”


A view from Vienna, day 5: Looking to the future

This week, Conor McKeever (our Research Communication Officer) is reporting from the European Association for the Study of Diabetes (EASD) conference in Vienna. Each day he'll be reporting on the things he's found interesting and exciting from Europe's biggest meeting of diabetes researchers.

Although things were winding down in Vienna, Friday was definitely a case of last but not least for type 1 research. Potential cures were at the forefront of the day’s lectures, with a particular focus on encapsulation and immune therapies – two big areas in which JDRF is investing.

Stanley Lasch, from the Goethe University Hospital in Frankfurt, announced the results from a study that combined two immune system treatments to make one more effective therapy. Current research into anti-CD3 drugs (which target the immune system T cells involved in type 1) has found that they can help reduce a person’s need for insulin, but that the effect wears off fairly soon after, allowing the T cells to return. Lasch’s team looked at adding a second drug that they believe can prevent T cells getting back into the pancreas after the anti-CD3 drug wears off.

Overall, 65% of the mice given the two drugs did not require insulin after six months; in contrast, 47% of the mice given anti-CD3 drugs alone did not require insulin after this time. Although research is needed to see if the effect can be replicated in humans, it’s an exciting step forward for a treatment that’s already receiving a lot of interest.

Dr Gerlies Treiber, of the Medical University of Graz, was also enthusiastic about a possible immune therapy for type 1. She has been investigating the effects of vitamin D on the immune system, as low vitamin D levels are one of the factors being studied as a potential contributor to type 1 risk. She found that giving vitamin D supplements to people who were newly-diagnosed with type 1 seemed to increase the activity (though not the number) of their regulatory T cells – the cells that are meant to stop the immune system attacking the body. Given that this defence appears to fail in type 1, increasing the strength or number of regulatory T cells is one aim of our cure research.

On the encapsulation side of things, Dr Evi Motté from the Diabetes Research Center in Brussels has been studying the effectiveness of the cells used in ViaCyte’s macro-encapsulation device. We recently announced how the company, which has received JDRF funding, now has approval to test their device in humans, so it was particularly pleasing to hear that other researchers are testing the cells ViaCyte use.

Motté found that the macro-encapsulated cells were able to secrete a much higher level of insulin than cells implanted using more traditional micro-encapsulation techniques. Levels were more similar to the levels found in non-protected transplanted cells, but non-protected cells are still vulnerable to attack from the immune system, so fail more quickly.

On the whole, the last day of the conference showed there is a lot of hope for cure research. Immune therapies and encapsulation work is coming on apace, and it’s really encouraging to see that researchers from around the world are getting behind the same work that JDRF is supporting. In fact, I’d say the same was true of the week as a whole – there’s so much tremendous research going on and there was barely a session that didn’t have JDRF-supported work somewhere in it. It’ll be great to see where the research goes from here, and I’m excited to see what will be announced at next year’s conference in Stockholm.

Photo: Vienna by Flickr user Miroslav Petrasko, used under a Creative Commons licence.


A view from Vienna, day 4: type 1 tech and treatments

This week, Conor McKeever (our Research Communication Officer) is reporting from the European Association for the Study of Diabetes (EASD) conference in Vienna. Each day he'll be reporting on the things he's found interesting and exciting from Europe's biggest meeting of diabetes researchers.

It’s hard to believe that the JDRF Artificial Pancreas Program was launched only eight years ago. Since then, we’ve gone from a few prototype devices being used by one or two people, to three-week and three-month trials of the artificial pancreas at home, unsupervised by researchers.

But as exciting and as close to reality the first generation devices are now, we’re not resting on our laurels. Thursday’s presentations from researchers focused on all elements of the artificial pancreas – CGMs, pumps and the algorithm – and how we can get the most from them.

Dr Hood Thabit and Dr Martin Tauschmann, both working as part of the University of Cambridge artificial pancreas team, were among those in Vienna to share their results.

They’ve found that using the artificial pancreas overnight helps people to bring their glucose levels down, without increasing the risk of hypos – a success that we’ve previously reported on. They’re also looking at why some people do better than others on the trials, to see what can be done to improve the efficacy of the device. At the moment, according to Dr Tauschmann, the longer a person has had type 1, the less time they spend in the target blood glucose range when using the artificial pancreas. If the researchers can establish why this is, they will use that information to make the device even better than it is currently.

Dr Thabit also discussed a CGM accuracy trial that had supported their decision to allow the artificial pancreas to be used at home. It was no small undertaking, taking the equivalent of 2,002 days’ use (nearly 5 ½ years!) for the CGMs being used to be deemed accurate enough. This, if anything, made it clear that the researchers are dedicated to making the best artificial pancreas system possible.

Later, we heard from Dr Roberto Trevisan of the Papa Giovanni XXIII Hospital in Bergamo, Italy, who has found that using insulin pumps can help people with type 1 avoid complications. Dr Trevisan’s trial suggested that even when blood glucose levels were similar to those of people using insulin injections, using a pump reduced the risks of kidney problems.

To round off the day, Professor Eric Renard, of the University of Montpellier, gave his opinion on whether ‘the dream’ of an artificial pancreas could ever become reality. Drawing together the histories of CGMs and pumps, from the unwieldy and inaccurate devices of the 70s and 80s, to the increasingly complex simulators of the last few years that have allowed the two devices to work together, he made it clear he believes the artificial pancreas is closer than ever.

“Closed loop insulin delivery at night is already safe, effective and sustainable in the home, while 24/7 use is feasible, with several trials ongoing,” he concluded.

Photo: Vienna by Flickr user Krister, used under a Creative Commons licence.


A view from Vienna, day 3: trying to make type 1 diabetes complications less complicated

This week, Conor McKeever (our Research Communication Officer) is reporting from the European Association for the Study of Diabetes (EASD) conference in Vienna. Each day he'll be reporting on the things he's found interesting and exciting from Europe's biggest meeting of diabetes researchers.

While a lot of the research we fund at JDRF is working towards a cure, we also want to help people who have type 1 to live longer, healthier lives until the cure is found. That’s why we fund a number of projects looking at preventing and treating complications, alongside work to make controlling glucose levels safer and easier. And from Wednesday’s sessions at EASD it’s clear we’re not alone in this: researchers from around the world were here to discuss their work on understanding diabetes complications.

A lot of the studies presented today focused on understanding what causes complications – if we can understand this, we may be able to develop strategies to address these root causes before complications develop.

Stijn Peeters, from Maastricht University, is focusing on the extracellular matrix (ECM) – essentially, the space between the body’s cells, and the molecules that are found there. He has found that people with type 1 tend to have higher than normal levels of molecules that break down the ECM. He also discovered that having high levels of some of these molecules is associated with conditions like retinopathy and cardiovascular disease. Although these molecules are part of the body’s way of getting rid of old and damaged parts, it seems like having too many could indicate a higher risk of complications. Knowing this, researchers may be able to identify steps we could take to reduce that risk.

Other researchers looked at different complications.  A team from Manchester led by Dr Steven Brown looked at the effect of diabetic neuropathy on something that on the surface doesn’t come up much in conversations about diabetes – falling down the stairs. People with nerve damage to their limbs had greater trouble balancing when going up and down stairs than people without this nerve damage. The team are now working to understand whether strength training and other interventions can help mitigate this risk for people who do develop nerve damage.

Being able to diagnose complications early is a key goal for many researchers. Dr Vincent Monnier of Cape Western Reserve University announced how his team had been able to link the fluorescence of collagen in the skin to a person’s risk of retinopathy and kidney disease. It certainly seemed like a novel way to test for a person’s risk of these conditions, and new ideas like this are incredibly important for the future.

The fact that getting the best possible glucose control is still the best way to reduce risk of complications seems to be reinforced by a study from Sweden looking at difference in rates of complications between people using insulin pens and those using pumps – the pump group were 43% less likely to develop fatal cardiovascular disease than the group using pens. The authors were rightly careful to highlight that pump usage alone probably doesn’t account for all of this risk reduction. Other important factors, such as the intensive education people in Sweden receive when they go on a pump, are likely to play an important role in the difference between the two groups. Unpicking these factors, and deepening our understanding of how to detect and treat complications if they do arise, mean that we can look forward to a future where complications of diabetes are less, well, complicated!

Photo: Park in Vienna by flickr user Ville Miettinen, used under a Creative Commons licence.