The Diabetes UK Professional Conference is underway. Read Day One of DRWF Research Manager Dr Eleanor Kennedy’s blog reports.
Just over a year ago, I was planning my trip north to Glasgow for the annual Diabetes UK conference but, as the spectre of Covid-19 started to loom large across the world, it became very clear that the conference was going to become one of the first casualties of the pandemic.
At the time, we had no idea that, over a year later, as we all continue to adapt to a “new normal,” the pandemic would still be a very large part of our lives. And, as I sit here at my computer, logging onto yet another online, virtual conference, I feel very demoralised. But in equal measure, I feel saddened that I never fully appreciated the brilliant feeling that is packing up and heading off to a conference where I will learn something new every minute of every day and where I will meet familiar faces to share a coffee or a glass of wine with.
But here we are - Diabetes UK’s Annual Professional Conference 2021 with a twist.
No longer a packed three-day jamboree of back-to-back sessions from early in the morning ‘til late afternoon. Instead, a two-week extravaganza of lunchtime and early evening sessions starting around 11am and wrapping up just after lunch. Then kicking off again around 5pm for another couple of hours.
What have I learned a few days into this new look conference?
Well, the first thing I am delighted to report is that the prize lecturers of 2020 who never got the opportunity to deliver their talks, are this year’s prize lecturers. Not the same I am sure for the speakers, however I’m glad that they are getting their respective moments in the spotlight.
Formerly DRWF-funded researcher Dr Sarah Richardson on the complex interplay involved in the development of type 1 diabetes
First up is Professor Sarah Richardson from the University of Exeter, who gave the first of the prize lectures – the RD Lawrence Lecture Award. To be eligible for this, the awardee must be actively working in the field of basic or clinical science in diabetes in the UK at the time of his/her election to the lectureship and he/she should have no more than 20 years' post-doctoral research experience when the lecture is delivered. Not only does last year’s, and hence this year’s, winner fit these criteria, it is delightful to know that Professor Richardson was the recipient of our Non-Clinical Fellowship back in 2010 and so is well known to us here at DRWF.
Professor Sarah Richardson
Professor Richardson began her lecture by reminding us that type 1 diabetes arises from a complex interplay of genetic, immune and environmental factors. Most patients presenting with type 1 diabetes have evidence of antibodies and immune cell responses against self. However, with more than 50 candidate genes associated with the development of type 1 diabetes and environmental factors like viruses, diet and exposure to vitamin D all viewed as potential triggers, the picture is far from clear.
Part of the problem in doing research on this is the access to tissue and Professor Richardson talks eloquently about the lack of human pancreas for research. Since the 1950s there have only been around 600 pancreas samples made available to the research community to study. These are divided into several cohorts but, interestingly, many of the newer cohorts of pancreases are from people who have donated their organs but who had had type 1 diabetes for a long period of time so the very active stages of immune attack, which reduces after the first year, is not so prevalent and therefore more difficult to interrogate in these tissue samples.
Key age-dependent differences in type 1 pathology include the type of immune cells present, the number of immune cells present, the levels of beta cell destruction and the processing of insulin. Professor Richardson explained that, although type 1 diabetes has one endpoint, it may actually be two health conditions as those with a younger age at onset (under 7 years of age) have many immune cells with the infiltrate containing a lot of B cells and CD8+ T cells that are key in the immune attack. They also have fewer residual beta cells at diagnosis that are lost rapidly and feature abnormal insulin processing. However, in the older age of onset group i.e. those over the age of 13-years-old, there are lower number of immune cells with the infiltrate containing fewer B cells and they appear to retain residual beta cell function for a much longer period.
Professor Richardson concluded her talk with some emerging evidence about the role of enteroviruses in the onset of type 1 diabetes. Some published evidence does exist, but the signal is quite weak, suggesting that only very few cells have been infected with the virus in question. To investigate this more robustly, a multinational collaboration called the nPOD-Virus Working Group was set up to assess in an unbiased and blinded way to look at the presence or absence of an enteroviral infection in the pancreases of nPOD donors with diabetes or evidence of islet cell autoimmunity, using different techniques and reagents and in different laboratories.
The results confirmed the presence of enteroviral proteins and enteroviral genome through a range of techniques as well as evidence of a host response to the virus. Unlike non-diabetic donors, pancreas from donors with type 1 diabetes with residual beta cells had multiple markers of viral infection supporting the existence of a low-grade, recurrent, or persistent viral infection that affects beta cells.
What is the future for type 1 diabetes research?
Well, there could be possible prevention strategies in people at high risk via an enteroviral vaccine or anti-viral treatments given to new-onset cases in order to slow the destruction of the beta cells.
But the message is clear – type 1 diabetes is not the same in everyone and this type of research is moving us towards a time when we will be able to offer more personalised treatments to individuals and inform clinical management pathways and, perhaps most importantly, it could help us to develop strategies that would allow people with type 1 diabetes to retain some beta cell function, even in small numbers, which is known to reduce the risk of complications, increase time in range and reduce both hypo- and hyperglycaemic episodes.
A very positive note to end on and not a bad start to the conference!
Further reports to follow – visit DRWF news page
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