The venue for this event is The Royal College of Pathologists
2 Carlton House Terrace is the home of the Royal College of Pathologists, a professional membership organisation, concerned with all matters relating to the science and practice of pathology.
Carlton House Terrace was constructed largely between 1826 and 1829 and it remains the property of the Queen. Its balconies overlook the Mall in Central London where Buckingham Palace stands
This is a Euroscicon Small Conference, an outline of the day can be found at
Obesity: a multi discplinary approach to the genetic influence on this global epidemic. After hearing an overview of the problem, speakers will give evidence based on the genetics of eating behaviour, its influence on childhood obesity and treatment ; genome wide association studies identifying genes with a role in obesity, molecular mechanisms underlying the central control of food intake and body weight; and an appreciation of genetic factors over the environment in obesity. Speakers will also inform us of diseases associated with obesity.
This event has CPD accreditation
Who Should Attend
Academic and Research Institutes: Group and Lab Heads, Postdoctoral Scientists and Research Students
Biotech and Pharma Industry: CEOs, Chief Scientists, Group Heads, Senior and Junior Scientists, Research
Clinical researchers, clinicians, nutritionists, GPs
9:00 – 9:45 Registration
9:45 – 10:00 Introduction by the Chair: Jane Cutler, UK
10:00 – 10:30 Gene-environment interactions in obesity
Dr Clare Llewellyn , University College London and King's College London, UK
Despite the ubiquitous ‘obesogenic’ food environment, not everyone is overweight. Genetic susceptibility to the environment is thought to explain some of the individual differences in weight, with differential appetitive responses to food, being implicated as the mediating mechanism. It has been hypothesised that individuals who inherit a more avid appetite, lower sensitivity to satiety and preference for energy dense foods, are more likely to overeat in response to the modern food environment and gain weight – i.e. ‘obesity genes’ influence adiposity partly through appetitive mechanisms. This talk summarises the evidence for genetic regulation of appetitive behaviours.
10:30 – 11:00 Candidate gene studies in obesity and related traits
Dr. Vimal Karani S, Centre for Paediatric Epidemiology and Biostatistics, UCL Institute of Child Health
Obesity is an heritable trait that arise from the interactions between multiple genes and lifestyle factors such as diet and physical inactivity. Hundreds of candidate genes for obesity-susceptibility had been identified through various approaches. With genome-wide association study (GWAS) data now available on numerous large cohorts, it has become possible to embed candidate gene studies within GWASs, testing for association on a much larger number of candidate genes than previously possible. The talk will highlight three main aspects: 1.Gene x environment interactions, 2.Candidate gene analysis using GWAS datasets and 3.Use of Mendelian Randomization approach to obesity traits.
11:00 – 11:30 Speakers’ photo then mid-morning break and trade show/poster viewing
Please try to visit all the exhibition stands during your day at this event. Not only do our sponsors enable Euroscicon to keep the registration fees competitive, but they are also here specifically to talk to you
11:30 – 12:00 Genetic studies of metabolic disease - extreme phenotypes and common disease
Dr Inês Barroso, Wellcome Trust Sanger Institute, Cambridge
In recent years, genome-wide association studies (GWAS) have led to a rapid increase in the number of loci known to influence type 2 diabetes and obesity risk. This has highlighted particular pathways and genes, previously unsuspected, as having an important role in disease predisposition. Further important insights are also emerging from whole-exome sequencing studies of more severe phenotypes where rare mutations can reveal important pathways that when malfunctioning can lead to disease. Insights from these approaches and future directions will be highlighted during the talk.
12:00 – 12:30 Considering obesity as a chronic brain disease
Dr Giles S.H. Yeo, University of Cambridge Metabolic Research Labs, Institute of Metabolic Science, Addenbrookes Hospital, Cambridge, UK
It is an inescapable fact that the underlying cause of obesity is a result of consuming more energy than you burn. The question that is more complex to answer is why some people eat more than others. Over the past 15 years, insights from human and mouse genetics have illuminated multiple pathways within the hypothalamus, brainstem and higher brain regions that play a key role in the control of food intake. We now know for example, that the brain leptin-melanocortin signalling pathway is central to the control of mammalian food intake. Intriguingly, it is becoming clear that in addition to engaging classical “neuropeptide/receptor” systems within the brain, leptin also rapidly modifies synaptic connections between neurons. There is also evidence for neurotrophins, which are critical in the development and maintenance of neuronal connections, playing a role in the control of energy homeostasis. However, although monogenic alterations in these pathways result in extreme Mendelian obesity, these remain incredibly rare. The major burden of disease is carried by those of us with “common obesity,” which to date has resisted yielding meaningful biological insights. Progress however, has been made with genomewide association studies. For example, sequence variants in the first intron of FTO (Fat mass and Obesity related) are strongly associated with human obesity and carriers of the risk alleles show evidence for increased appetite and food intake. Although global FTO null mice display decreased fat and lean body mass, increased metabolic rate and food intake, this is seen against a complex phenotype of postnatal growth retardation and mortality. In contrast, when we modulated FTO levels discretely in the hypothalamic arcuate nuclei of adult animals, we were able to influence food intake, suggesting tissue specific functions for FTO. FTO’s physiological role and how it influences bodyweight is yet to be determined. Using a variety of in vivo, in vitro and biochemical methods, we are currently characterising the molecular mechanism by which FTO controls of energy balance. Further GWAS have now revealed more than 30 different candidate genes, most of which are highly expressed or known to act in the CNS, emphasizing, as in rare monogenic forms of obesity, the role of the brain in predisposition to obesity.
12: 30 – 13: 30 Lunch and trade show/poster viewing
13:30– 14:30 Question and Answer Session
Delegates will be asked to submit questions to a panel of experts. Questions can be submitted before the event or on the day
14:30 – 15:00 Genetics of obesity: A low- and middle-income country perspective
Dr Branwen Hennig, MRC International Nutrition Group at the London School for Hygiene & Tropical Medicine, UK and MRC Keneba, The Gambia
15:00 – 15:30 Afternoon Tea
15:30– 16:00 Associations between genes, lifestyle factors and glucose metabolsim in adolescents
Dr Alice Kong, The Chinese University of Hong Kong, Hong Kong
Type 2 diabetes is a multifactorial disease involving the interplay between gene and environment. We aimed to investigate the associations between dietary intake of vegetables, exercise, combined genetic risk score (CGS) and glucose metabolism in a community recruited cohort of adolescents. From 270 subjects who had undergone oral glucose tolerance test (OGTT) and genetic studies, we found a linear relationship between CGS and 2-hour post OGTT plasma glucose values. However, when these adolescents were stratified by their exercise levels and consumption of vegetables and fruits, the linear relationship was attenuated. Our results suggest that high exercise level and increased dietary consumption of vegetables reduce the risk of having high post-prandial glycemia which might be conferred by the genetic variants.
16:00 – 16:30 Non-alcoholic fatty liver disease: the hepatic consequence of obesity and the metabolic syndrome
Dr J. Bernadette Moore, University of Surrey
Non-alcoholic fatty liver disease (NAFLD) is now the most common liver disease in both adults and children worldwide. A disease spectrum, NAFLD may progress from simple steatosis to steatohepatitis, advanced fibrosis and cirrhosis. Development of NAFLD is strongly linked to components of the metabolic syndrome including obesity, insulin resistance, dyslipidaemia and type 2 diabetes. The cellular and molecular aetiology of NAFLD is multi-factorial; genetic polymorphisms influencing NAFLD have been identified and nutrition is a modifiable environmental factor influencing NAFLD progression
16:30 – 17:00 A Meta-analysis including 18,290 individuals confirms an interaction effect between depression and FTO genotype on BMI
Dr Margarita Rivera Sanchez, MRC SGDP Centre, Institute of Psychiatry, King's College London
This work focuses on exploring the influence of the FTO gene, BMI and depression concurrently in a meta-analysis including 18,290 individuals. A history of depression moderates the effect of FTO on BMI, such that the BMI-increasing effect is significantly enlarged. This meta-analysis demonstrates a consistent effect of the interaction between FTO, depression and BMI, and suggests that FTO is involved in the mechanism underlying the reported association between obesity and depression. It will also have implications for predicting which patients with depression are at risk of high-BMI related disorders and potentially highlights how to improve prevention, management and treatment programs.
17:00 Chairman’s summing up
The Deadline for abstract submissions for oral presentation is Feb 10th 2013
Abstracts for poster presentation only can be submitted up to two weeks before the event
There will be a best poster prize.
You can download the instructions for authors at
Keywords: genetics, obesity, diabetes, cardiovascular, NAFLD,Nonalcoholic fatty liver disease; proteomics; iTRAQ; biomarkers, genome-wide association studies; whole-exome sequencing; genetics; type 2 diabetes; obesity, Africa, life-course anthropometry/obesity, nutrition, developmental origin of health and disease (DOHaD) hypothesis, Childhood obesity; twins; appetite; genetic; behaviour, Obesity, Body mass index, physical activity, interaction, Mendelian Randomization, Genes, Lifestyle factors, Glucose Metabolism, depression, obesity, BMI, FTO gene
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