EASO ECN-EASD ECA: Collaborating Across Obesity and Diabetes

Description

This EASO ECN-EASD Early Career Academy joint webinar explored the value of collaboration between the obesity and diabetes research and clinical communities. Speakers highlighted the shared challenges across both fields, and emphasised how interdisciplinary collaboration can strengthen research, improve patient care, and support career development. Presentations also introduced early career opportunities within both networks, including education, networking, and collaborative research platforms. The session provided practical insights into how early career professionals can engage across disciplines to enhance impact.

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Transcript

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Speaker 1 • 00:00
Hello everyone, good afternoon. It is my great pleasure to welcome you on this month’s ESO Early Career Network e-learning hub. Today we have a great opportunity to take part in a collaborative webinar between the ESO Early Career Network and the ESD Early Career Academy me. And this webinar will be focusing on collaborating across obesity and diabetes. We will have also a great pleasure to hear a talk of one of the leading researchers in this field, Professor Kirfi Pietilainen from Helsinki. And all of us will have opportunity to ask questions at the end of the webinar during the last approximately 15 minutes. But before For then, we introduce you briefly the activities of our networks from my side from the ESO Early Career Network and my co-host Alfredo, who I would like to welcome with this way, would briefly introduce and outline the activities and possibilities that are offering through the participation in the Early Career Academy from the ESD. I would like to state that the Novo Nordisk Foundation has provided support for ESO for ECN development activities, including also these webinar theories. However, the Novo Nordisk Foundation has had no influence over the content. My name is Martin Schoen. I’m a member of the ECN at ESO. I originally come from Slovakia, but currently I work as a physician in the University Hospital in Dusseldorf in Germany. I would like to also introduce Alfreda as my co-chair from ESD Early Career Academy. I would like to remind you that this webinar is being recorded and also that the recording will be posted in the ESO video archive soon after the event so you will be able to come back and watch the webinar again. You will have the opportunity to ask questions obviously that would be answered at the end of CareFif talk. We would have approximately 15 minutes and for the questions please use the Q&A function through the webinar and at the end we would pick the questions and we would answer them mostly on the first come first basis. At the end, at the very end of the webinar, you will be asked to complete the feedback that appears after the webinar. Your comments are very valuable for us to improve and to meet your expectations for the future webinar. So we would appreciate if you could take a moment and dedicate a little bit of time to complete this feedback. Now I would like to introduce Alfredo as my co-chair from ESD Early Career Academy.

Speaker 2 • 03:08
Hi everyone, I’m Alfredo Catturano and I’m an Assistant Professor of Internal Medicine at San Raffaele Roma University in Rome and I’m part of the ESD Early Career Academy. The ESD Early Career Academy is an initiative of the European Association for the Study of Diabetes with the aim of for supporting and empowering early career clinicians and researchers throughout education, mentorship, networking and research opportunities. I’m really, really happy to be here today for this joint webinar between the EASO and the EASD that brings together two strong early career communities in the field of obesity and diabetes. I will now hand over to Martin, who will present on early career opportunities in obesity and diabetes from the ASO perspective.

Speaker 1 • 04:11
Thank you, Alfredo, for the kind introduction. So I would like to start with presenting a couple of slides introducing and especially highlighting the benefits that are provided from being a member of the Early Career Network that is an organization or association that is tightly connected with the European Association for the Study of Obesity. So during this couple of slides, we would highlight the opportunities for members of this network that are practically lying, especially lying in providing educational platforms. for example like in this webinar that you are taking part right now, but also a lot of opportunities to network and to establish new connections for the future research or maybe also for the future career. So who can become a member of the early career network of the ESO? The eligibility criteria meets all of those who are currently enrolled or recently completed relevant undergraduate or postgraduate degree, but also those who hold or would be applying for some entry-level position, either in academia, in research, in the NGO or public health organization. So the eligibility criteria, as we can see, are quite broad and all of people who could meet these criteria are encouraged to apply and maybe take some advantage or contribute to early career network by the ESO. This membership includes benefits such as monthly webinar for a lot of educational events, educational platforms, but also activities at the European Congress at Obesity that is approaching and taking place in a couple of weeks in Istanbul. But members are also eligible to apply for awards, for some travel grants, to get some support, for example, to attend the ECO, but could also be a member of the WhatsApp group in order to share activities, maybe some know-how and again opportunities to network. One of the main activities that our network is providing and organizing is taking part in these e-learning hubs, for example, the webinar that are conducted on a monthly basis and you are right now taking part in one of such where usually we invite one of the leading figures in a dedicated topic to deliver a keynote lecture. Another activity that we are providing is organizing of the ECN Masterclass, which is also educational event that takes place on an annual basis, usually in November, during two or three days, where young researchers from the field are provided for educational platform to discuss the hot topics, to have some learning opportunities through interactive pathways and get some maybe also soft skills, but also practical skills that they can apply in the future research. Here is a picture from the previous very successful ECN masterclasses. and we have also a couple of activities during the European Congress on Obesity taking place in one month in Istanbul. During this Congress, we will provide a couple of networking events. We will also have the ECN Lounge, where you can come by, to buy in person a network, but also we will be also holding some ceremonies for the awards and also for the grant applications. One of the awards that we give on an annual basis includes the ECN Best Thesis Award. So all members of the ECN network are eligible to apply and submit their thesis with some justifiable impact of their research on an obesity-related field. We would select three finalists that would have the opportunity to present their research session during the ECO and also would be eligible to win the price of 500 euro each. Usually the application period is until the middle of January. Apart from that, our network is also coordinating a new investigator award, which is a grant opportunity for young researchers to apply for in four key areas that include basic science as well as clinical research, childhood, obesity and public health. And the awardees could receive grant support of up to 300,000 Danish crowns, which equals to approximately 40,000 euro to fund their research in obesity. Similarly, then with the Bethesda Award, each winner would have the opportunity to present the research during the European Congress on Obesity. We also provide in collaboration with ESO some travel grants for those of you who are interested to join the European Congress on Obesity with accepted abstracts. The support for the travel and accommodation cost can be up to 500 euro and along with that you would receive also the complementary registration. And one of the activities that ECN is providing on the social platforms is, for example, ECN Spotlight on a regular basis where we highlight and present the background but also research focus and some interesting findings of selected researchers, young researchers of the field which is again a growing opportunity how to maybe also network, but also get inspired from peers working on a similar topic and doing something similar for the future. We are very active on the social media, for example, on the LinkedIn, but also on other commonly used social media such as Facebook, Twitter. And also we have this WhatsApp group that we previously mentioned. You can scan this QR code in order to become a member and access all these benefits and opportunities that we just presented in the previous slides. Now I would like to hand over to Alfredo, who would briefly introduce us the benefits and the opportunities provided by the Early Career Academy from the ESD.

Speaker 2 • 11:25
Thank you very much for your overview and insight. I’m trying now to share my presentation. I have many things on the other side. Sorry. Okay. That’s perfect. Okay. I will now present the early career opportunities in obesity and diabetes from the ESD perspective. But first, what is ESD? It is one of the leading European scientific societies in diabetes with more than 20,000 members worldwide with the aim of promoting research, education and clinical care. ESD is also the organizer of the UNED meeting, the last one was held in Vienna in 2025 and We have more than 13,000 attendees and around 2,000 presentations coming from all over the world. But what is important is what the ESD can do for your career. And there are four main pillars, which are education, research support, networking and career development. Education is one of the longstanding core mission of the ESD. In fact, we have a committee made up of 10 members coming from all over Europe and with different expertise. Then we have an e-learning platform to disseminate knowledge and proficiency. And we have also meetings and courses that are divided by application or by invitation. And there are also joint sessions and collaborations with the local, regional and global partnership to share experience in diabetes research, education and care. About meetings, I want just to take you the opportunity of two main courses which might be of interest for you. And it is the Robert Arner Clinical Research Training course, the one I participated in 2023. It is held in Oxford, and we had the opportunity to improve our knowledge about clinical research and have some basics about statistics and how to use R. And since then, I’m using R for all my statistical analysis. And then we have also the scientist training course, which is more basic science-oriented one, and where you can stay in the lab and do some research with beta cells and be trained with the basics to do that. We have also, as ESD, a lot of research opportunities with a lot of support. There are grant programs that are supported by Lilly and Novo Nordisk and Sanofi. And of course, we have also programs for young investigators that are mainly travel fellowship program, reciprocal travel research fellowship program, and also a future leader in the diabetes field. And the Rising Star Symposium with the Rising Star Fellowship. That if I don’t remember wrong, Martin was one of the winners for this. Then we have also the Early Career Academy with the aim of to further support, train and mentor and for scientists and clinicians and students who are at the early or intermediate stage of their career. We organize mainly webinars, journal clubs, we try to bring together junior clinicians or researchers with established mentors through a mentorship and then we would like to foster the networking. The networking is especially performed during our social events at the annual meeting which are lively interactive networking sessions with a great opportunity to hang up with the others, share ideas, create collaborations and also have fun and in a relaxed setting with some drinks or food. And science is important but networking is even more important and that’s what we do at the annual meeting. There are also the early career academy prize winners and sorry, and we try to give some prizes to eight young researchers who presented their works at the annual meeting. We also host webinars and journal clubs and sometimes also workshops together with the postgraduate education committee. And about the mentorship program, as I mentioned before, this is an opportunity for bringing together early career scientists and expert leaders in order to accelerate the network development. Up to now we have provided around 70 mentorship programs with 1000 euro each to help them and around 40 have already been completed it is one year opportunity you have the opportunity to uh get uh in uh we discuss with the men a mentor from uh all over the europe about some problems also life issues because what we care most is life work balance and sometimes uh due to research we have to move from one place to another so sometimes it could be uh really problematic so if if you choose a mentor and you such as this problem, you can share, you can try to share also these things and to get some feedback. And you can use also this 1000 euros for travel expenses if you want to go to our mentor labs. That is what I’ve done because I won the mentorship program in the 2023 and I went to Professor Jargoida within Prague and stayed there for three months. Of course, €1,000 is not enough. But in my case, it was really, really crucial because I wanted to go abroad during my PhD studies and I was facing a lot of troubles. And the mentorship program helped me getting to know Professor Jargoida and go to his lab. and the three months there were wonderful. Then we also have activities of the Early Career Academy that are meetings. We had the first meeting last year, and it was held in Pisa, and this year it was at DDZ in Dusseldorf a few weeks ago. During this event, we try to foster networking between researchers from everywhere. We also provide prizes for the best abstract winners. We try to make you deliver to the best abstract deliver a speech so that you can also practice to be on the stage. And we try to do one or two workshops according to the time we have allocated. And we have leading experts coming from all over Europe to deliver their speech and to foster a collaboration and also the discussion with them. And we are also more active on social media. You can scan this to get in touch with us. You can follow us on Instagram, LinkedIn, or just mailing us. The take-home messages from the ESD is that you need to start early, be proactive, apply for opportunities and build your network. Because ESD gives you the tools, but your career depends on how you use them. And thank you. I’ll now pass the leading role to Martin for the rest of the meeting.

Speaker 1 • 20:24
Alfredo, thank you very much for the very thoroughful presentation about the great activities that ESD Early Career Academy is providing and offering. and now it is my great pleasure to move forward and to move on and introduce Professor Kirsi Pietilajnan who is a professor in clinical metabolism at the University of Helsinki as well as chief physician at the Helsinki University Hospital. Professor Pietilajnan focuses in her research in bridging the genetics and environmental factors that contribute to development of obesity and also related metabolic disorders with a particular emphasis on twin studies in order to better understand the mechanisms behind weight regulation. Kirsi published so far approximately 300 peer-reviewed articles and according to Google Scholar, her work reached approximately 35,000 citations. Apart from that, Kirfi also received some major competitive fundings, including grants from Council of Finland as well as Novo Nordisk Foundation. And last but not least, Professor Pietilainen also leads the Center for Obesity Management, which is promoting translational research at the clinical level. And she also made some major contributions to clinical guidelines for obesity and related metabolic disorders. So, Kirsti, it is a great honor and we are very much looking forward for your talk.

Speaker 3 • 22:16
Thank you, Martin, for your absolutely wonderful words. and thank you IEASO and EASD for this wonderful opportunity. I think that it is absolutely wonderful that you are bringing in people from both the fields of obesity and diabetes, and it is essential for us to collaborate, so I’m super glad to be here today. I am very honored as well, and let me share my presentation and also start with a little story. I hope that you can see my slides now. And please, if anything is wrong, let me know. So I actually think that the EAZO early career network may have begun in 2005 when I was having, I was going to these EASO meetings, ECHO meetings, with my mentor, with my supervisor Aila Rissanen, who was a very wise woman and she knew everybody. We were walking on the corridors and we were meeting all the important people in the EASO community. And I was talking to Aila and I was saying that, look, I don’t know if I know anybody from my own age group, which was 21 years ago. So, Aila then suggested that why don’t we talk to Jyön? Jyön Woodward is the executive director of IEASO. And then Jyön warmed immediately to this idea that why don’t we bring in the young people? So that’s what we then did, 2005 in Athens meeting. That was the very first meeting. We were called Young Investigators United at that time, but now the early career network maybe better illustrates on what the whole point is. But I’m so, so glad that how far you have gone, how good you’ve become and how well connected you’ve become and this very webinar where you are now together with EASD is a prime example of this, I think. So Martin and Alfredo, do you see my whole screen or do you see something else?

Speaker 1 • 24:40
We see your screen. Yeah. All right. We can see the screen.

Speaker 3 • 24:44
Okay, good. So now I’m, this is like an old lady memorizing things, but now something that came to my mind when I was preparing for this presentation was indeed my career as a young medical doctor around 20 or more than 20 years ago, which was the variability in people. So I had patients with obesity and they were all lovely people and they were all very individual. And also I realized that their metabolism was highly different. So here you have two females, same age, same BMI and two males, same BMI, same age. But when I measured their metabolism back then, I realized that they were very different. So here’s the one female on the left who has a BMI of 34, 20 years old. And here are the glucose and insulin curves after the oral glucose tolerance test. Same age, same BMI, female, again OGTT. you can see a little bit different curve in glucose but especially a very different curve in the insulin response. Same thing for these males. Look, same age, same BMI males. Here’s the glucose curve and here are the insulin curves. So now you can realize that these people despite the same BMI all have very different paths towards diabetes. They may all be there to develop diabetes one day but their paths are very different and they are in a very different stage in their journey. So then because I am a twin researcher, I also study twins and I often found that when I have monozygotic twin pairs, I do an oral glucose tolerance test or any kind of a test, meal test, glamping, anything to these twins and their metabolism is usually like exactly the same which you can see in here. Then also what we did back then was that we studied how well connected are individual people’s BMI to their risk for diabetes. This is a big cohort of individual people of course this is actually a twin study but here you can see that if you have a BMI of around 20 to 25 your risk for diabetes is not very large but it progressively already starts to increase And then when your BMI is around 35, your hazard risk for diabetes is 30 times higher. So that in itself speaks for the connection between diabetes and body mass index. But also both obesity and diabetes are actually quite heritable. So when we estimate based on twin studies the heritability of these conditions, you can often end up to percentages that are way more than 50%. So then this brought us to this idea that, well, if you can say that obesity both maybe causes diabetes, but also both of these conditions are heritable, so how on earth are you going to distinguish them from each other? How can you distinguish the genes from the environment? And that will be very difficult when you are studying any individual people or any random people. But then when we actually have monopsychotic twins, we can also take a look at a very special study design where we have identical twins, monopsychotic twin pairs, but their BMIs now differ. So that’s what we then did together with Aila, who was my vice mentor. We contacted Professor Jaakko Caprio, who in Finland has a 50-year record of collecting twin studies. And we went through all Jaakko’s twin pairs, which were at that time around 8,000 twin pairs. So in these large cohorts of twins, what we did, we tried to find all monopsychotic twin pairs. One third of them were monopsychotic. Among these twin pairs, thousands of twin pairs, we were trying to find everyone whose BMI differed for more than 3 kg per unit. And also their weight then differed for more than 10 kg. But actually trying to find such twin pairs was very difficult as you can see. We started with thousands of twin pairs and we ended up in 50 pairs, which to you then already tells that obesity is very genetic. It is very very difficult to find identical twins who differ in their BMI a lot. Nevertheless, we were then able to find these 50 twin pairs and we did a range of metabolic studies within these twin pairs. So first of all, on average the twins had about 17 kilograms weight difference and in the heavier coat twins they had more fat in every compartment that we measured. Of course, epicardial fat was one that we measured. We measured magnetic resonance imaging subcutaneous adipose tissue, there was more of course in the heavier co-twins, more visceral adipose tissue, more pancreatic fat and most astonishingly as much as 380% more liver fat was in the heavier co-twins to this 17 kilogram weight difference. That then translated into lower insulin sensitivity. This was clamping that we did for the twins and also there were many measures of chronic low-grade inflammation circulating in plasma that were increased in the heavier coat twins. Now next what we then wanted to zoom into was the liver fat because we were astonished about the high liver fat content in the heavier coat twins and then we went and looked at these more closely and what we actually found was two very distinct groups of twins. One group of twins where you could see that despite this 17 kilogram weight difference on average, this group 1 was such that the heavier co-twin did not have excess liver fat. Not at all. The liver fat percentage was close to 1%. So these twins had normal liver fats despite their obesity. But then this other group was this more normal obesity group, you can see that the excess weight then resulted in a huge increase in their liver fat compared to the leaner co-twins who nearly always had normal liver fats. And then this brought us these group one and group two kinds of twin pairs. And then we went on and measured many things. Here you can see the liver fats in a bar format and then we measured for example in MRI these subcutaneous and visceral abdominal fat contents and then you can see that there was similar amounts of subcutaneous adipose tissue in these twin pairs whereas in the visceral adipose tissue there were clear differences. So there was increased visceral adipose tissue also in the so-called healthy group, but really the group where there was large large liver fat increases, then that was the group where the visceral adipose tissue also was predominantly increased. Then what we did, in this study we did OGTT, we also did clamps, but this is OGTT, where you can also see that now if group 1 twin pairs were similar for liver fat, they were, remember, different in body weight, 17 kilogram on average, but similar in liver fat. So liver fat then seems to determine the fact that their glucose is similar. And also insulin levels were surprisingly similar in these twin pairs. But now in this group 2, where remember the heavier had more liver fat, so in this case then this translates into higher glucose in the heavier and higher insulin in the heavier. And then interestingly, we went and collaborated with Professor Jens Holst in Denmark, who invented the GLP-1. So in this study, we then found that measuring GLP-1 after a meal test or after an OTTT, we realized that in this healthy group, so to say, where the heavier one did not have excess liver fat, they also had increased GLP-1 compared to their lean compartments. However, when the liver fat was increased, in this case, the heavier co-twin, who was more metabolically compromised, also had lower GLP-1. And every one of you knows now that GLP-1 is a useful gut hormone, supporting your satiety and supporting your glucose homeostasis. Then what we also did, we took adipose tissue biopsies. And this really started the whole entire career for me for adipose tissue. And what we then found was that the single most important down-regulated adipose tissue pathway that was different between the lean and the heavy co-twins on average was mitochondrial pathways. So we did the transcriptomics results at first and then here we found out that if you have your lean group here measured as this reference value and compared to that you have every twin and the heavier twin then you can see that when I took this number one down regulated pathway which was mitochondrial oxidative phosphorylation, these were nearly always downregulated in the adipose tissue of the heavy coat twins. Here you can see the same thing, but this is gene by gene. Now there are around 100 genes in this oxfos pathway. Blue means that it’s low in obesity, it’s low in the heavier coat twins compared to the leaner coat twins. And then we were thinking that, well, this is very surprising because adipose tissue, what has mitochondria even have to do in adipose tissue? And then we took some electron microscopy pictures and we realized that mitochondria in adipose tissue are sitting right next to the lipid droplet, which then made us think that well mitochondria might support the lipid droplet accumulation, so that if mitochondria are working poorly, then lipid droplets are not formed. This then means that adipose tissue is not formed properly and maybe thereby not having proper mitochondria in adipose tissue results in ectopic fat deposition. This is the hypothesis that we made and indeed that was true. Remember this figure and we found out that indeed when we compared again the metabolism of these two groups, we found out that the group with the high liver fat, they also had in their adipose tissue low mitochondrial gene expression pathways and they had inflammation. But when we then had this group where there was no difference in liver fat, there was also absolutely no difference in the adipose tissue gene expression pathways. So what we could see here is that this is the so-called healthy group, healthy obesity group. And this tells us that even if obesity often results in many metabolic disturbances that are leading to diabetes, it is very heterogeneous and liver fat is determining and adipose tissue, mitochondrial and inflammation pathways are determining whether you will have your obesity more likely to develop towards diabetes. Then the other side of the story was our weight loss studies. We’ve done different weight loss studies, many of them, but I will just tell you that one of the most recent ones, which was bariatric surgery study. So we actually in this study, we did a comparison, direct comparison for two different bariatric surgery methods. One was the Roux-en-Y gastric bypass, which is here, and one is one anastomosis gastric bypass, which anatomy is shown here. So here, instead of this normal Roux-en-Y gastric bypass, where you cut the jejunum here and lift it up to this small pouch, what you here do is that you kind of make this stomach like a sleeve, like longer, but small stomach pouch, and then you don’t cut the jejunum, you just lift it here. Anyways, this was the thought of our surgeons and we then collaborated in doing metabolic studies. We measured many things. This is a study published by Sini Heinonen and us. So these are the two groups of operations and the main message here maybe is that there were no differences in these two operation types in terms of metabolism or body weight change. Here you can see that weight loss is about almost 30% in both cases, there’s fat loss, there’s a little bit of lean body mass loss as well, and also there is a very drastic, very rapid loss in liver fat, which is expected. And then we saw many things that other people have also seen in terms of bariatric surgery, how useful it is for metabolism. We saw decreases in fasting glucose, fasting insulin, HbA1c, HOMA index, increases in MADS, a little bit decreases in total cholesterol, increases in HDL, decreases in LDL, decreases in triglycerides and decreases in inflammation status. So this is all known. But then we also went to study the bariatric surgery effect on adipose tissue. This is actually another study. This was published by Birgitta van der Kolk and Mahesh Muniandu. And this was a collection of different European cohorts. So we had a lot of collaborations in this study who had collected the bariatric surgery cohorts. But what we here did, we took adipose tissue biopsies and again, we measured RNA sequencing transcriptomics. And here we saw that the actual reverse happened after bariatric surgery for the mitochondrial pathways. So they were highly, highly upregulated after surgery. And here you can see all the results by gene and by time point. These are time points on up to five years and everything being red means that nearly all of the genes highly upregulate after surgery. So now we are looking into what might explain this result. Of course, the mere weight loss can be a factor, but when we measure different weight loss studies, we didn’t see the same effect. Only bariatric surgery induces this. And maybe it is the metabolic effects of bariatric surgery, not the mere weight loss, that increases the mitochondrial activity. And then, well, this is just one proof that metabolism and gut hormones really change after the bariatric surgery. This is the very study where we randomized to these two operation types. And here you can see GLP-1. What is very, very important for everyone, every clinician to understand that a patient who is here starting bariatric surgery, this is baseline measures. This is BMI about 40, 45. they don’t have GLP-1 secretion. You give them a meal, this is a meal response, and there is no GLP-1. Now, if you do bariatric surgery very soon, this is six months and this is 12 months, you can see that the GLP-1 goes from zero to 100 in 15 minutes. Well, we know this, but I think that clinically, this is a very important message for everybody. already for obesity, but the more you go towards diabetes, the more suppressed the GLP-1 response to meal is. And this is, I think, the message that we can deliver that de-stigmatizes our obesity. It’s not their fault that they don’t have satiety after a meal. It’s the biological response. Alright, so now I’m coming to the end of my presentation. And just to summarize that what would be the single most important insight from this session? I would think that obesity and type 2 diabetes, they are not two separate stories. They are chapters of the same metabolic narrative, but it’s very heterogeneous. So what you need to do, you need to study every patient individually, not assume that every patient with obesity has every metabolic condition. Also, by treating obesity, you can already then treat type 2 diabetes. Why would it be particularly relevant for early career professionals working across obesity and diabetes? I think that the most impactful science, the most impactful scientist in the next 10 years will be those researchers who are fluent in both obesity and diabetes medicine. And what concrete action, mindset or collaboration should you as early career researchers take forward? I would think that being curious, believing in your own data, following on what your own data shows you, that will be very, very important. You can talk to different people, different communities, maybe something outside your own box. And that will always be educative. And also, I think, as Alfredo said, have fun. Sometimes the best collaborations start from the dance floor. I have personal experience on this. So thank you very much for this opportunity and good luck with the early career networks and academy. Thank you.

Speaker 2 • 44:31
Thank you very much, Professor Pietilainen, for this excellent and insightful presentation. We now move to the discussion and I would like to remind the audience that you can continue submitting your question through the question and answer function. I’ll start with the first question. That is, we are collaborating across obesity and diabetes here. What other areas should our early career researchers aim to connect with to enhance care for people living with these diseases?

Speaker 3 • 45:12
What other areas? The line was breaking a little bit. So what other areas?

Speaker 2 • 45:17
Yeah, other areas except for people living with obesity and diabetes that should be prioritized by early career researchers.

Speaker 3 • 45:28
Well, because I am an obesity researcher, I myself tend to think that obesity is like the life in a miniature in the sense that if you have obesity as your interest area, then you will immediately then be connected to diabetes, cardiovascular disease, arthrosis, osteo, whatever, and also mental disorders. So it is like a window for you for different things and also in your clinical experience You can then then take a look at many many things I think that diabetes in a sense is the same So if you have diabetes in your interest you already then do have this your patients will have cardiovascular issues. They will have Mechanical osteoarthritis issues. They will have psychiatric issues So the whole field of medicine is then open to you. And by the way, I will forward my slides to my acknowledgments and my thank you to my collaborators. And I will leave you with this lovely picture with my team members. And I especially want to thank all of these wonderful researchers in my team.

Speaker 1 • 46:44
Thank you, Kirsti, for a wonderful and very stimulating talk for all of us. We can continue with a couple of questions from the queue and I. One person is asking, thank you, Professor Pietilainen, as an early career researcher in a small lab, how can I strike up a collaboration with the lab in a different country, especially if the lab has a different specialty from mine? Thank you.

Speaker 3 • 47:15
Yeah, well, that is a very good question. Of course, going to congresses and then showing activity in congresses, ECHO and EASD is the important ones. So you will find your peers. I was finding it very useful that I, of course, had my mentor. It was very easy for me because then I already met people not from my own generation, but maybe the other generation too. For you to actually collaborate, you would maybe need to connect different generations. But to start with is to form connections with the peers of your age and the peers of your interest. It will come. If it doesn’t come immediately, this Congress, it will come eventually. So be persistent, be curious, be active, be glad, be friendly, be, you know, the good guy in the field so that everybody will in the end know you. It will pay off, I’m sure. But then, of course, you can search for your interest area. The Internet is, of course, full of knowledge nowadays, so to contact directly, you might be lucky in that. But I think that personal, like having an actual physical presence in these meetings, I think is crucial for people to get to know you, people to trust you and then moving on from there.

Speaker 1 • 48:51
Maybe the dance floor is an answer and opportunity. We have also a question from Alessandra. After bariatric surgery, some patients regain weight. How do they behave in terms of the oxfords expression after regaining the weight?

Speaker 3 • 49:13
Oh, that is an excellent question. We don’t actually know that. So, in weight regain, the major thing is the appetite. So, major fault kind of in the body is that the appetite suppression diminishes. And that is the driving force. It can be that it is a mere decrease in gut hormone secretion in the end, after five years, after some years after aging. It might be that it is this physical, or it can be that it is psychological. It can be that it is the very same problems that were there in the first place, now coming into play again. And it can be a mixture of many things. Also, what I would like to highlight here is a clinical tip that it might be due to glucose variation. So this reactive hypoglycemia, which people after bariatric surgery often experience so that their glucose increases very highly and then insulin increases. And then after two hours, you are in hypoglycemia. Now you feel hungry. Now you feel that, OK, this urge to eat. Your hands are shaking. you are feeling low glucose and you are eating carbohydrates, more carbohydrates, which then only presents with more insulin and another spike. So that might be that this nibbling and this carbohydrate overload is the one that then makes you body weight regain. Well, however, back to this original question about what happens to adipose tissue, what happens to the mitochondria? Well, nobody knows. I would guess that weight regain is connected to decrease in the original increase in the mitochondrial activity, but we don’t know. But nevertheless, the brain response, I would think, is the primary thing for weight regain.

Speaker 1 • 51:20
Maybe just a follow-up question. Do you think the GLP-1 could be a solution for these hyperglycemia peaks after the bariatric surgery, like adjuvant therapy for those who just had this kind of surgery?

Speaker 3 • 51:36
Yeah, yeah, important question. That is what we then do and that is what we use. However, I would encourage us clinicians to really examine thoroughly what is the case. If it’s psychological issues that are driving you to eat too much carbohydrates, you can, of course, suppress it pharmacologically, but you would need to examine that why is the person then maybe craving for more carbs than he or she should be. And also to examine the really the metabolic basis in the sense that take proper lab tests, take vitamins. There’s usually deficiencies in ferritin and vitamin D, vitamin B12, such things, anemia, which are connected to poor diet and maybe poor. What is this ingest, you know, absorption of the nutrients? Anyhow, it’s a very complicated thing. But what we end up doing in the end is like both having GLP-1 injections to our patients, experiencing weight regain and also then supporting them psychologically, supporting them with nutrition and physical activity.

Speaker 1 • 52:49
Thank you very much. Another question came from Jens. Is it known why these pairs of monozygotic twins are disconcordant for BMI, maybe epigenetics or something else?

Speaker 3 • 53:04
Yeah, again, a very good question. So we did actually, maybe Bram, would you care to actually come to air if you are there? Maybe that would be an option too, but because Berenson has been studying the twins very carefully himself as well.

Speaker 4 • 53:25
Oh, wait, is it? Yeah. Okay. Um, well, I have not specifically looked at, uh, you know, um, DNA methylation, but I think some colleagues have right. Kiersey. Um, I believe there have been some, some minor differences, but, but quite small actually. Um,

Speaker 3 • 53:48
Yeah, that’s true. And then the parts that you studied, then, Bram, are maybe more relevant. So if we are thinking twin pairs, they will have 50 different reasons for their difference. But mainly it is it’s actually quite difficult to fetch what is it. But it can be related to food habits and physical activity and sleep and mental health habits still. But epigenetics, because we had the weight curve such that the twins were of similar body weight until around 16 to 18 years of age. Thereafter, the weight began to depart. And then what we had, the epigenetics was like at 25 years remark. So then there were small differences. But it was the outcome of obesity, I think, rather than the reason for all these discordances.

Speaker 4 • 54:45
Yeah, that’s the thing. I mean, so in my thesis, I did see that the twins with the higher BMI have to take slightly fewer steps in a day. They sleep a bit less. They eat slightly unhealthier, but the differences are quite small. And again, the question remains, is that the reason for the difference or is the consequence of the BMI difference? And we don’t really know.

Speaker 1 • 55:13
The next question came very long way from Tanzania. Thank you very much for joining us, Lucy. Lucy has been living with type 1 diabetes for over 20 years, and she’s also advocate and journalist and the founder of Diabetes Consciousness for Community. And she would like to ask if there is any scientific evidence showing that insulin use can actually lead to weight gain in people who use it and also at the same time obesity is known to be one of the causes of type 2 diabetes

Speaker 3 • 55:48
well that is a very very very tricky question what we see is that every every group of people actually do gain weight nowadays and balancing with with the with with insulin amounts in type to type 1 diabetes is it’s not an easy task because you also you want to control your glucose and then the minute you eat a gram of too much glucose then you need more insulin and then it can lead to weight gain. Also reverse weight loss in type 1 diabetes is also not very easy because of the balancing for the correct carbohydrates and insulin amounts. But does it then, insulin is adipogenic, but does it cause obesity in type 1 diabetes? I think it’s It’s not easy to say that this would still be the case. Or what do the other clinicians think? Alfredo, Martin, what do you think?

Speaker 2 • 57:06
Well, actually, I believe that everything comes from what you eat, because if the carbohydrate intake is too much, you need more insulin. Insulin has anabolic effects and, of course, adipogenesis. So you can do whatever you want as a type 1 diabetes. We have also athletes that win medals at Olympic Games. It depends on your behavior. And of course, it is really hard to lose weight once gained in type 1 diabetes due to this fact. Because as long as you increase your weight, you will need more insulin. It depends also on the sensibility to insulin, because generally if I have a young person living with type 1 diabetes, he may not be insulin resistant, but once he gains weight, he can become also insulin resistant. So it’s really hard to answer. But yes, there is a link between adipogenesis and insulin use. I believe the right solution is what you eat, do physical activity because it’s good for your health. What do you think, Martin?

Speaker 1 • 58:24
I agree. It’s very important to also distinguish the diabetes phenotype, not only the type, because there is huge heterogeneity when it comes to type 1 and type 2 diabetes. so like to have the special phenotypic profile together with the lifestyle factor. So I think that should be addressed on a very individual level and it’s like difficult to draw like general conclusions on this topic. The next question, maybe we have time for one last, came from Ivan who asks: How do you explain different results in weight loss between people with obesity without diabetes and people with obesity and diabetes in therapy with GLP-1 receptor and loss?

Speaker 3 • 59:16
Yeah, this is highly, highly interesting question. I wish I knew the answer. Could it be that there is some kind of resistance to weight loss in a person with type 2 diabetes? Could it be that it is brain-related somehow? Could it be that low-grade inflammation or the metabolic status of the excess glucose or excess something in the blood then interferes your ability to decrease eating? That is, I think, one possible explanation. But of course, we don’t know. We don’t know with a physical activity whether that consuming energy part is also different. And in many diabetes studies, one has to remember that the drug studies are done such that the lifestyle intervention is actually not very intense. However, in any obesity related trials, even if the type 2 diabetes is in the primary population, there should have been this intensive lifestyle advice as well. So many different. I hope we find the answer. you or you you can you can be the one to do that yeah i think that’s very interesting topic

Speaker 1 • 01:00:34
in general and we definitely need more data coming up from clinical studies maybe the last question thank you for presentations how can i with the public health master of navigate my way in obesity and diabetes research I think there are definitely opportunities maybe on the epidemiological level. On statistical level there is also big room to implement and to advocate for policies in terms of translational research. um kirk i don’t know if you have um maybe some further opinion on this question for a student with a public master degree

Speaker 3 • 01:01:27
yeah we have we have many we have many master’s degree researchers as you in the obesity community i think well uh it’s because obesity is so broad diabetes is so broad maybe you need to then focus on what is the real interest in there. But I myself, for example, before I became a medical doctor, I was a nutritionist. So already then I found that, well, I could have studied research on obesity. Maybe not exactly examining patients, but there are many, many, many, many cohorts who need expertise. So the world is full of data. So we only don’t have enough investigators to analyze them. So I’m sure there will be a room for everyone.

Speaker 1 • 01:02:21
So I think that’s a great answer for the maybe last question and great room and motivation for all of us to navigate ourselves into harvesting more data and to be able to analyze them and work with them. Kirfid, it was a great pleasure to have you here and thank you very much for the fantastic talk. and very stimulating discussion at the end. I would like to also thank all the fellow panelists that helped to organize this fantastic webinar. And thank you all for joining. Also, thank you for Alfredo for co-hosting this collaborating even between the ESO Early Career Network and the ESD Early Career Academy. Again, thank you, Professor Pietilajnen, for the excellent presentation and to both our early career communities for our engagement and also thoughtful questions.

Speaker 5 • 01:03:25
Thank you, everybody. Thank you, Marcel and Alfredo. Thanks, everyone. Thanks, everybody.

Two ECO2026 Prizes Open for Applications Until 5 May

Economics of Obesity and Metabolic Health Summit

EASO ECN-EASD ECA: Collaborating Across Obesity and Diabetes

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