MINUTES OF THE 44th GENERAL ASSEMBLY OF

Diabetologia (2009) 52:[Suppl1]S1–S550 DOI 10.1007/s00125-009-1445-1

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MINUTES OF THE 44th GENERAL ASSEMBLY OF THE EUROPEAN ASSOCIATION FOR THE STUDY OF DIABETES held in Rome, Italy on 10 September 2008 at 18:15 Present:

E. Ferrannini G. Spinas M. Stumvoll E. Gale V. Jörgens and 42 members

(President) (Honorary Treasurer) (Honorary Secretary) (Editor-in-Chief, Diabetologia) (Executive Director)

The President welcomed everyone to the 44th General Assembly. 1. MINUTES 43rd GENERAL ASSEMBLY 2007 Since there were no comments, the minutes were approved unanimously and officially signed as a correct record. 2. REPORTS a) President The President reported on the joint project with EPA, ESC and EASD to prepare a statement concerning cardiovascular risk in diabetes in patients with severe mental illness. The President confirmed that the Foundation was continuing to flourish. At present, 16 EFSD programmes are in place and meetings have been scheduled in Rome with potential new partners. b) Honorary Treasurer The Honorary Treasurer reported that the positive balance was mainly due to an increase in the number of registered delegates and an increase in the interest accrued. The expenditure in 2007 increased due to the increase in the amount spent on the salaries and the expenditure

for the Annual Meeting. It had been decided to transfer 1.7 million to the Foundation. Dr. Spinas said that of the Foundation’s total income more than 90% was spent on research. Dr. Spinas expressed his thanks to Drs Grüßer and Jörgens for their support and advice and to the team in Düsseldorf in general and to Mrs Klee and Ms Deparade in particular for the precise handling of the accounts. The President thanked the Honorary Treasurer for his diligence and asked if there were any questions. There were none. c) Honorary Auditors The President asked the Honorary Auditor, Dr. Tiedge, to formally discharge the accounts. He confirmed that the accounts had been checked carefully and were in perfect order. Dr. Ferrannini asked for the vote to accept the accounts. The accounts were accepted unanimously (one abstention). d) Honorary Secretary Dr. Stumvoll reported that he had restructured some of the groups and the committee; there are now 40 reviewers to score 8 topics. Of the 2498 abstracts received,

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1402 had been accepted. This number was then divided into 264 orals and 1138 posters. He said the Programme Committee was already in place for the Annual Meeting in Vienna and it would convene later that day. Dr. Stumvoll closed his report by thanking all members of the EASD staff, in particular Mrs H. Goliberzuch and M. Toledo, for their outstanding help and support with the organisation of the EASD Annual Meetings. Dr. Ferrannini thanked Dr. Stumvoll for his diligence and asked if there were any questions. There were none. e) Editor-in-Chief, Diabetologia Dr. Gale reported that a total of 1769 articles had been submitted to Diabetologia in 2007, which was a slight increase over 2008. The median time from receipt to first decision was 17 days. The acceptance rate for all article types combined fell to 17.4%. The impact factor rose to 5.8. He expressed his thanks to the referees and associates and said their work was much appreciated. He also thanked his team in Bristol. Dr. Ferrannini thanked Dr. Gale for the excellent work he had done. He said a sub-committee had been appointed by the Executive Committee to evaluate potential candidates for the position of Editor-in-Chief. There were no questions. f) Chair, Postgraduate Education Sub-committee Dr. Nolan reported that the usual postgraduate courses had taken place in Jena, Loipersdorf and Wroclaw. The course planned for Belgrade has been postponed until 2009. A course is being planned by Dr. Mankovsky in Ukraine. Regarding web-based education, 2 pilot sessions on standard topics were held in Düsseldorf in 2008. Further web-casts are planned including hypertension and diabetes, diabetes and the heart and type 2 in adolescents and children. Dr. Nolan thanked the team in Düsseldorf, especially Mrs. M. Hata and Mr. B. Carey, for their friendly assistance. Dr. Ferrannini thanked Dr. Nolan for his valuable work. There were no questions.

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Diabetologia (2009) 52:[Suppl1]S1–S550

3. ELECTIONS a) President 2008-2011 The council’s election of Dr. U. Smith was unanimously approved with one abstention. b) Vice President 2008-2011 The Council’s election of Dr. A.J.M. Boulton was unanimously approved with one abstention. c) Editor-in-Chief extension 2009-2010 The extension of the Editor-in-Chief’s term of office until 2010 was unanimously approved with one abstention. d) Honorary Auditors 2008-2011 The Council’s election of Drs. K. Paterson (UK) and C. Tack (The Netherlands) was approved with 1 abstention. c) Council Members 2009-2012 The following Council Members were unanimously (1 abstention) elected by the General Assembly: J.-M. Boavida (P), C.-G. Östenson (S), A. Pfeiffer (D) and N. Wareham (UK). 4. STUDY GROUPS Dr. Stumvoll said that the Study Group Forum which had been held on 7 September had been well attended and no problems had arisen. 5. HONORARY MEMBERSHIP Drs. J.-P. Assal and R. Unger were unanimously elected by the General Assembly. 6. MEMBERSHIP FEE The General Assembly unanimously approved the proposal that applications for membership of EASD starting on 1 July would run for 1½ years.


7. ANY OTHER BUSINESS There was no other business. Dr. Ferrannini thanked the out-going Vice President, Dr. U. Smith, for his dedication and presented him with the Albert Renold Medal. Dr. Smith expressed his thanks for the confidence that had been shown in him when he was elected President. Dr. Smith warmly thanked Dr. Ferrannini for his outstanding service to the EASD as President and handed over the Albert Renold medal.

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Dr. Ferrannini thanked the industry for their support. He also expressed his sincere gratitude to the Local Organising Committee for their outstanding contribution to the organisation of the 44th EASD Annual Meeting. He again thanked Dr. Stumvoll and the members of the Programme Committee for their hard work with regard to the scientific programme. The President warmly thanked the EASD team in Düsseldorf for their kind and efficient help. Dr. Ferrannini brought the General Assembly to a close at 18:35.

Dr. Ferrannini also thanked the outgoing members of the Council: Drs. K. Dahl Jørgensen, B. Mankovsky and S. Sasson.

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Agenda for the 45th General Assembly of the European Association for the Study of Diabetes to be held in the Basch Hall at the Messe Wien, Vienna, Austria on 01 October 2009 at 18:15 1. Minutes of the 44th General Assembly, Rome, Italy 2008 2. Reports a) President b) Honorary Treasurer c) Honorary Auditors d) Honorary Secretary e) Editor in Chief, Diabetologia f) Chair, Postgraduate Education Sub-committee

Dr. U. Smith Dr. G. Spinas Dr. K. Paterson Dr. C. Tack Dr. M. Stumvoll Dr. E. Gale Dr. J. Nolan

3. Elections a) Vice President 2009-2012

in place of Dr. C. Boitard

b) Editor-in-Chief 2010-2013

in place of Dr. E. Gale

c) Honorary Treasurer Extension 2009-2010

Dr. G. Spinas

d) Chair, PGESC Extension 2009-2010

Dr. J. Nolan

e) Council Members 2010-2013

in place of Dr. F. Ashcroft (UK) Dr. F. Bosch (E) Dr. V. Petrenko (LT) Dr. A. Siebenhofer (A)

4. Study Groups 5. Honorary Membership 6. Any other business

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45th EASD Annual Meeting of the European Association for the Study of Diabetes Vienna, Austria, 30 September – 2 October 2009

Abstracts Index of Oral Presentations

Index of Poster Sessions

OP 1 GLP-1 in the treatment of type 2 diabetes mellitus OP 2 Prediction and prevention of type 2 diabetes mellitus OP 3 Diabetes education and management OP 4 Diabetes and the heart OP 5 Genes, autoimmunity and type 1 diabetes OP 6 Inflammation, insulin action and type 2 diabetes OP 7 Beta cell regeneration and loss OP 8 Diabetic nephropathy and blood pressure OP 9 Diabetes in childhood OP 10 Retinopathy OP 11 Fatty acids and lipids OP 12 Protecting beta cell mass and function OP 13 Type 2 diabetes mellitus genetics and genomics OP 14 Endothelium and coagulation OP 15 Glucose monitoring OP 16 Metabolic effects of bariatric surgery OP 17 Diabetes and pregnancy OP 18 Molecular mechanisms of type 2 diabetes mellitus and obesity OP 19 Tissue stress and response OP 20 Beta cell biology OP 21 Insulin action – animal models OP 22 Responses to GLP-1-based therapy OP 23 Epidemiology of type 2 diabetes mellitus and cardiovascular risk OP 24 Effects of maternal diabetes and childhood obesity in diabetes OP 25 Cognitive function and type 2 diabetes mellitus OP 26 Mechanisms and markers of cardiovascular disease OP 27 The secretory machinery OP 28 Inflammation, obesity and metabolism OP 29 Novel therapies for type 2 diabetes mellitus OP 30 Neuropathy OP 31 Insulin sensitivity, adiposity and risk assessment OP 32 Clinical immunology OP 33 Incretins OP 34 Life and death of beta cells OP 35 Obesity and adipose tissue OP 36 Insulin therapy in type 2 diabetes mellitus OP 37 To amputate or not to amputate OP 38 In vivo insulin action – mechanisms OP 39 Healthcare delivery OP 40 Monogenic diabetes and obesity OP 41 Insulin secretion in vivo OP 42 Metabolic effects of incretins

PS 1 Genetics of type 1 diabetes PS 2 Prediction and prevention of type 1 diabetes PS 3 Type 1 diabetes – epidemiology PS 4 Prediabetes and screening for type 2 diabetes PS 5 Prevalence of type 2 diabetes PS 6 Epidemiology of cardiovascular disease PS 7 Epidemiology of obesity and type 2 diabetes PS 8 Replicated genes for diabetes and obesity PS 9 Genetic variation in type 2 diabetes PS 10 Genetic variation for metabolic traits related to type 2 diabetes and obesity PS 11 The role of genomics and metabolomics in drug response PS 12 Cytokines and ER stress in beta cells PS 13 Signalling of beta cell damage PS 14 Oxidative stress and ROS in beta cells PS 15 Beta cell lipotoxicity PS 16 Experimental type 2 diabetes PS 17 Experimental insulin secretion PS 18 Beta cell transcription factors and transporters PS 19 Beta cell transcriptional regulation PS 20 Ion channels in beta cells PS 21 Beta cell – exocytosis PS 22 Beta cell metabolism PS 23 Stem cells and beta cell development PS 24 Islet and pancreas transplantation PS 25 Immunoprevention in type 1 diabetes PS 26 Markers of autoimmunity in type 1 diabetes PS 27 Immune modulation in diabetes PS 28 Action of insulin and its analogues PS 29 Insulin sensitising agents – animal studies PS 30 Insulin sensitivity in adipose tissue and muscle – human studies PS 31 Clinical physiology of insulin sensitivity PS 32 Insulin sensitivity and lipids PS 33 Pathophysiology of insulin resistance PS 34 Insulin sensitivity – animal studies PS 35 Glucagon – secretion and effects PS 36 Incretin secretion in humans PS 37 Insulin secretion in vivo PS 38 Incretin secretion – studies in animals PS 39 Hypoglycaemia in type 1 diabetes PS 40 Hypoglycaemia PS 41 Glucose metabolism - experimental PS 42 Metabolic effects of various hormones PS 43 Sex hormones and metabolism

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PS 44 Systemic inflammation in obesity and diabetes PS 45 Adipose tissue and adipocytes PS 46 Regulation of adipose tissue inflammation PS 47 “Metabolic syndrome” – clinical and experimental PS 48 Liver pathophysiology and metabolism PS 49 Fat depots and body composition PS 50 Brain / CNS and metabolism PS 51 Linking exercise to metabolic effects PS 52 Clinical and mechanistic aspects of therapeutics PS 53 Lipid effects and metabolism PS 54 Adipokines – „classical“ and novel PS 55 Secretory function of adipose tissue PS 56 GLP-1 agonists – clinical 1 PS 57 GLP-1 agonists – clinical 2 PS 58 DPP-IV inhibition – clinical PS 59 Incretin-based therapies – cardiovascular risk factors PS 60 Incretins – safety PS 61 Incretins pharmacology and pharmacokinetics PS 62 Incretins – experimental PS 63 Incretins – mechanisms of action 1 PS 64 Incretins – mechanisms of action 2 PS 65 Nutrition – experimental PS 66 Nutrition PS 67 Prediction and prevention of type 2 diabetes mellitus – 1 PS 68 Prediction and prevention of type 2 diabetes mellitus – 2 PS 69 Risk factors for type 2 diabetes mellitus PS 70 Insulin sensitisers 1 PS 71 Insulin sensitisers 2 PS 72 New therapeutic targets and therapies PS 73 Diabetes in childhood PS 74 Insulin analogues PS 75 Clinical aspects of oral medication PS 76 Clinical aspects of insulin therapy PS 77 Safety of insulin therapy PS 78 Continuous glucose monitoring PS 79 Glucose measuring devices PS 80 Pump treatment PS 81 Improving insulin PS 82 Technical aspects of insulin delivery PS 83 Starting insulin in type 2 diabetes PS 84 Type 1 diabetes – clinical aspects PS 85 Insulin therapy – type 1 diabetes PS 86 Diabetes education PS 87 Depression in diabetes PS 88 Psychological aspects of diabetes PS 89 Diabetes in the hospital PS 90 Diagnostic tools PS 91 Health care delivery PS 92 Health economics PS 93 Nephropathy – experimental PS 94 Nephropathy – clinical 1 PS 95 Nephropathy and treatment effects PS 96 Predictors of nephropathy PS 97 Nephropathy – clinical 2 PS 98 Hypertension

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PS 99 Hypertension – clinical PS 100 Eye complications PS 101 Retinopathy – experimental PS 102 Retinopathy PS 103 Autonomic neuropathy PS 104 Neuropathy and wound healing – experimental PS 105 Diabetic foot PS 106 Somatic neuropathy – clinical PS 107 Gestational diabetes – pathophysiology PS 108 Gestational diabetes – maternal and foetal outcome PS 109 Pregnancy – complications PS 110 Intrauterine development and observations in children PS 111 Treatment in nephropathy, hypertension and macrovascular disease PS 112 Other complications PS 113 Macrovascular complications PS 114 Rodent models for experimental diabetes PS 115 New therapeutic options PS 116 Statins PS 117 New therapeutic options PS 118 Fatty liver PS 119 New insights into lipid and lipoprotein function PS 120 Lipids and metabolism PS 121 Endothelial dysfunction PS 122 Oxidative stress PS 123 Cardiovascular disease – epidemiology and detection PS 124 Clinical management of vascular disease PS 125 Diagnosis and management of vascular disease PS 126 Biomarkers and assessment of cardiovascular disease PS 127 Cardiovascular disease - early detection and prevention PS 128 Cardiovascular disease and diabetes PS 129 Non-conventional risk factors for cardiovascular disease


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OP 1 GLP-1 in the treatment of type 2 diabetes mellitus

Conclusion: In this study, 1-year of EX therapy, compared to IG, significantly improved both the prandial ISR over a range of glucose concentrations and the potentiation of the ISR to glucose dose-response relation. The beneficial effects on the dose-response relation were sustained after a 5-week off-treatment period in both the EX and IG treated groups. Supported by: Amylin Pharmaceuticals, Inc., Eli Lilly

1 One-year exenatide treatment improves beta cell response in metformin treated patients with type 2 diabetes which is sustained after 5 weeks discontinuation of treatment M.C. Bunck1, A. Mari2, A. Corner3, B. Eliasson4, R.M. Shaginian5, Y. Wu6, P. Yan6, R.J. Heine1,7, U. Smith4, M.-R. Taskinen3, H. Yki-Jarvinen3, M. Diamant1; 1 Department of Endocrinology / Diabetes Center, VU University Medical Center, Amsterdam, Netherlands, 2Institute of Biomedical Engineering, Padua, Italy, 3Department of Medicine, Helsinki University Central Hospital, Finland, 4Lundberg Laboratory for Diabetes Research, Sahlgrenska University Hospital, Goteborg, Sweden, 5Eli Lilly, Houten, Netherlands, 6 Amylin Pharmaceuticals, Inc., San Diego, United States, 7Eli Lilly, Indianapolis, United States.

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Background and aims: Recently we reported exenatide (EX) improved hyperglycaemic clamp derived measures of ß-cell function, compared to insulin glargine (IG) in metformin (MET) treated patients with type 2 diabetes. Here we report the effect of EX treatment on the ß-cell response to a more physiological stimulus, i.e. a mixed meal. Material and methods: In this investigator-designed study, we compared the effects of both EX and IG treatment on prandial ß-cell function during an 8 hour, high fat, double mixed meal test. Sixty-nine MET treated patients with T2D (pre-treatment (PT) age 58±8y; HbA1c 7.5±0.8%; BMI 31±4kg/m2 [mean±SD]) were randomised to EX (n=36) or IG (n=33). Meal tests were performed at PT, after 51-weeks on-treatment and again after 5-weeks offtreatment on 59 patients (EX: n=30; IG: n=29) who received a breakfast at t=0h and lunch at t=4h both containing approximately 50g fat, 75g carbohydrates, and 35g protein.C-peptide deconvolution was used to calculate insulin secretion rates (ISR), and a mathematical model to obtain the dose-response relating ISR to glucose concentrations (bGS=glucose sensitivity=dose-response slope; ISR@Gref=ISR at reference glucose level [Gref]) and a timedependent potentiation factor expressing a relative potentiation of the doseresponse relation during the meal (POT; [time]-to-basal potentiation ratio). Results: After 1-year treatment, EX resulted in a greater upward shift in ISRgref than IG (between group geometric LS mean ratio±SE: 1.41±0.17, P=0.007 ([email protected]); 1.32±0.16, P=0.025 ([email protected]) and 1.26±0.15, P=0.060 ([email protected])). Additionally, EX treatment increased POT after both breakfast and lunch meals compared to IG (between group geometric LS mean ratio±SE: 1.22±0.11; P=0.026 and 1.19±0.11; P=0.054, for [170-190min]-tobasal and [240-480min]-to-basal respectively). Both Ex and IG treatment equally improved bGS (median[IQR] change from PT: EX: 7.9[2.2-27.5], P