In gut we trust; the importance of microbiota (#DPC16)
I have been lucky enough to spend the last couple of days at Diabetes UK’s Professional Conference at the SECC*. Anyone who follows me on Twitter cannot failed to notice this; over 450 Tweets and counting; sorry my normal intermittent service will resume shortly.
Gut Microbiota
One of the joys of being at the conference is the amount of interesting science being discussed and disseminated. One of the the first themes amongst these to catch my eye was Gut Microbiota. These are a complex community of over a 100 trillion micro-organisms which influence our physiology, metabolism and nutrition (you might also hear the descriptions gut flora, microflora or gut microbiome). An increasing volume of research data has made it to the public attention of late, with mentions in Newspapers and on TV in recent months.
What intrigues me about this subject is that it offers an opportunity to better understand some of the everyday differences People With Diabetes (PWD) observe in the impact of food on our Blood Glucose (BG) levels; put three PWD around a table and you will hear three different accounts of how their bodies respond to particular foods.
We are not all the same
Medical textbooks and lore have long suggested that some foods (e.g. white bread) give everyone an abrupt spike in BG, whereas other foods (such as wholegrain rice) give everyone less of a spike. This is sometimes referred to as the Glycaemic Index (GI) of a food, and there is a large amount of published data on which foods have a large impact on BG (e.g. “High GI”) and which have a lower effect (e.g. “Low GI”). Like many people I have always wondered why my experience didn’t match the textbooks. A bit of digging shows that the standard size for group of people on whom the GI tests are performed has long been just 10, none of them PWD.
More recently published research is now coming to light, especially the work of Weizmann Institute using much larger groups has demonstrated not only that everyone is very different, and that explanation for this lies in differences in our gut microbiota.
The gut, microbiota and diabetes
A couple of things surprised and excited me about the conference session on the 3rd March. The first was that my assumption that this was going to be about how we digest food was entirely wrong, and secondly that there is broad research under way about the relationship between diabetes and gut microbiota that I was completely unaware of.
In the first presentation of the session, Susan Wong (Professor of Diabetes and Metabolism at Cardiff University) asked “Do Gut Microbiota play a role in Type 1 diabetes?”. She explained that gut microbiota are important in how our immune systems develop, and demonstrated that there were many ways in which microbiota can interact with a person and hence it is possible that they can influence some diseases. Research in mice has shown that an imbalance in microbiota can be a cause of Type 1 Diabetes (T1D), Professor Wong suggested that this could also be true in humans, although this was not supported by research at this time. This led to a discussion about the possibility of changing microbiota in humans, but as there has not yet been any study on antibiotics and probiotics on T1D risks, it was too early to say what this might mean for the prevention or treatment of diabetes in the real world.
Gut microbiota in Type 2 diabetes
In the second presentation of the session, Patrice Cani (Université catholique de Louvain) who’s motto is "In Gut we Trust"! which I have blatantly stolen for the title of this blog** talked about the role of gut microbiota in Type 2 Diabetes (T2D). He started by demonstrating that in T2D PWD the gut microbiota varied significantly to those in people without T2D, and that through changing the microbiota living in mice alone (i.e. no change in diet) skinny mice could be made obese. This work has led to a treatment for obesity in mice (lucky mice!) but a lot more work would be needed before this was applicable in humans.
Metformin and the gut
In the final presentation of this session, Professor Ewan Pearson (University of Dundee) talked about the famous and infamous drug used for the treatment of T2D, Metformin. This drug is the front-line treatment for T2D in the UK, and can also play a significant role in prevention of the condition. It is infamous because of the side-effects that many users experience when it is first prescribed. The most common of these are nausea, vomiting, diarrhoea, nausea, vomiting, and flatulence (a couple of these get a double mention based on my personal experience).
Professor Pearson did not question the effectiveness of the drug, but challenged the conference's understanding of how it works, and suggested some ways in which knowledge of microbiota can explain the common side-effects. He also demonstrated that there is a genetic disposition in some people to particularly severe side effects, and suggested how screening for this could significantly improve the patient’s experience for a significant minority of newly diagnosed PWD.
In this presentation, and across the others in the session, one particular microbiota got mentioned a lot; Akkermansia muciniphila. It will be interesting to look out for future references to this, as it is widely believed to have anti-inflammatory effects in humans and having higher abundance in your gut is associated with reduced likelihood of inflammatory conditions such as appendicitis or irritable bowel syndrome. It is far from clear whether this is significant in itself, or whether this is the result of another unknown process, but either way we are likely to hear about this again soon.
What does this mean for PWD?
This session was very much about basic science; building our understanding of microbiota and the effects they have, and it is clear that a lot more research is needed on a wide range of fronts to give us a clear understanding of the role microbiota may play in diabetes (of all types). What I did find encouraging is that there are early signs that this work could unlock not just better understanding, but the potential for transformative prevention and treatment solutions for diabetes.
* Disclosure; I attended the DPC 2016 as a guest of Diabetes UK, who paid for my hotel accommodation.
**I was going to write my own gags, but I just couldn’t stomach it…
