Report from Day One of the European Association for the Study of Diabetes 2019
DRWF Research Manager Dr Eleanor Kennedy blogs from the opening day of the EASD conference.
This year’s European Association for the Study of Diabetes (EASD) meeting is in the beautiful Catalonian city of Barcelona.
Nestled on the coast of the Mediterranean Sea, this is a bustling and cosmopolitan city home to Antoni Gaudi’s fantastical and famously still unfinished cathedral masterpiece, the Basílica de la Sagrada Família.
The EASD congress attracts around 15,000 delegates from more than 130 countries making it one of the largest international conferences on diabetes research in the world.
The programme runs over four days of packed sessions. More than 1,200 talks and presentations will be given by a range of researchers from junior PhD students and postdoctoral fellows to leading experts and key international opinion leaders in the field announcing landmark clinical trial results.
And whilst this is fabulous for those of us who live and breathe diabetes research the big question is which session do I choose to go to? At any one time, there will be up to six parallel streams of talks but, as I head into the massive Fira Barcelona Conference Centre, there is only one session on. The Opening Ceremony followed by the Presidential Address.
Gaudi's Sagrada Familia in Barcelona
The president of EASD this year is Professor David Matthews, a very well-known face to those of us working with DRWF as he is the current chairman of our Research Advisory Board that oversees the grant funding rounds that we have in the UK.
Professor Matthews gives a typically barnstorming performance keeping an audience of several thousand raptly engaged.
The main event of the morning, however, is the award of the Claude Bernard Prize Lecture which, this year, was awarded to Professor Steve Kahn from the University of Washington in Seattle, America.
Unravelling beta cell dysfunction in type 2 diabetes
Professor Kahn’s talk is entitled Unravelling beta cell dysfunction in type 2 diabetes: from the unpredicted to the unknown.
Professor Kahn starts his talk with a quote from the Claude Bernard, the French physiologist after whom the award is named who is considered to be the founding father of modern physiology: “When we met a fact which contradicts a prevailing theory, we must accept the fact and abandon the theory, even when the theory is supported by great names and generally accepted.”
The talk ambles through his impressive research career starting with data demonstrating the failure of the beta cell to enhance insulin release with the development of insulin resistance result in hyperglycaemia to what he terms the unpredicted.
Normal glucose tolerance is maintained by the beta cell appropriately modifying insulin output in response to changes in insulin sensitivity or so-called “compensation”. The “decompensation” opposite effect is the failure of the beta cell to enhance insulin release with the development of insulin resistance which results in hyperglycaemia on all racial and ethnic groups. And, as the majority of type 2 diabetes genes are associated with beta cell dysfunction, this all underscores the central role of the beta cell.
Science is “we”
Claude Bernard also said: “Art is I; science is we” – an artist can very often create something by him- or herself. But a scientist never can and Professor Kahn highlights the importance of multidisciplinary teamwork that allows bodies of work such as his to form over the years.
It’s a salient point and it is something that I am sure I will be reminded of throughout the course of this meeting. No piece of work is done in isolation and, in the diabetes world, we are extremely fortunate to have friends and colleagues throughout the world who collaborate with one another to push research ever forward.
Type 2 diabetes and young people – a growing problem
Another topic that Professor Kahn touches on and one that is highlighted in other talks across Day One is the growing problem of type 2 diabetes in youth. The SEARCH for Diabetes in Youth study has shown an increasing incidence of type 2 diabetes particularly in Native American and non-Hispanic Black and Hispanic communities.
Obese youth with early type 2 diabetes are more insulin resistant and have hyper-responsive beta cells compared to adults with similar glucose tolerance profiles and, interestingly, the insulin resistance in these obese youth is unresponsive to metformin alone. And, again, in contrast to adults, despite medical intervention, in youth, beta cell dysfunction progressed significantly throughout the study.
By the time I limp into one of the last sessions of the days, we have covered almost every aspect of diabetes treatment and management at some point during the day but, in keeping with the lecture that kicked off this year’s EASD conference, I look into beta cell replacement.
As Professor Kahn’s lecture stressed the decline of the beta cell, I finish with beta cell replacement and another prize lecture.
Beta cell replacement
The recipient of this year’s Albert Renold is Professor Timo Otonkoski from the University of Helsinki in Finland. Professor Otonkoski is a former member of the Research Advisory Board for our sister organisation, Diabetes Wellness Sverige in Sweden. His elegant work on stem cells includes work on human embryonic stem cells which are still the gold standard of human pluripotent stem cells and which have clinical therapeutic applications in a number of different disease areas as well as induced pluripotent stem cells, a much newer stem cell model.
Professor Otonkoski’s research encourages me that, yes, whilst we know that the beta cell in decline is at the heart of type 2 diabetes, there are so many additional strands of research being woven together to give us a more in-depth understanding of what is fundamentally driving this decline and how we can, perhaps, overcome it. But it is the drive of the researchers involved in all of the work that I have heard presented today that has impressed me so much.
So, roll on, Day Two, Barcelona! You already have much to live up to!
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