Some impressions from EASD September 2015

easd2015

This year’s inspiring meeting of the European Society for the Study of Diabetes in Stockholm gathered nearly 18 000 participants who could choose from 1,209 of 2,067 submitted abstracts presented at 48 oral sessions and 123 poster sessions, 35 symposia with 95 invited top researchers from all around the world as lecturers and five award lectures.

The research presented spanned from basic research to the clinic, genetics, pathophysiology, epidemiology and treatment studies. Some highlights were:

Hans Häring from the University of Tübingen held this year’s Claude Bernard lecture which was a brilliant presentation of forefront research in the pathogenesis of type 2 diabetes. His group has studied how liver fatty infiltration can trigger inflammation and via fetuin A affect insulin resistance in other organs. They have also investigated how perivascular fat influences upon the vasculature in the various organs involved in diabetes pathogenesis. He described a new mouse model of obesity without inflammation and studies of the brain’s importance for the development of insulin resistance and obesity. The group has studied the relationship between hyperglycemia and insulin resistance in the mother and brain activity in the fetus. Their working hypothesis is that insulin resistance in the brain starts early (in utero) and is the cause of obesity and type 2 diabetes.

During the joint symposium organized by EASD together with the European Society of Cardiology entitled “Lessons learned from glucose lowering trials” a lively debate arose when epidemiologist Professor Craig Currie went far in drawing conclusions about cause and treatment consequences from observational epidemiological studies. Professor Lars Ryden, a cardiologist from Karolinska Institutet, led the session, which gave a broad overview of the status in the field.

The highlight of the Congress was still unquestionably the presentation of the results of the EMPA-REG study Thursday afternoon. Great expectations were raised as it was preannounced that the study came out positive on the primary endpoint and the article in the New Engl J Med was released while the results were presented. The results showed that treatment with empagliflozin over 2.6 years reduced the primary endpoint (the combination of cardiovascular death, nonfatal myocardial infarction and nonfatal stroke) from 12.1% in the placebo group to 10.5% in the groups receiving empagliflozin 10 or 25 mg (considered collectively). Even more impressive was that the drug reduced both cardiovascular and total mortality significantly, 38% and 32% respectively. Empagliflozin is thus the only among the new antidiabetic drugs that has shown significant positive effects in randomized controlled long-term studies with ‘hard endpoints’. Like all good research studies, also this study raises many new questions. Although the drug has a positive impact on blood sugar, blood pressure and weight, these effects are modest. And based on the Kaplan-Meyer curves, we can see that the effects on outcomes appear very early after the start of the study – far earlier than one would expect if the mechanism of effect was that the treatment reduces atherosclerosis. For the present, we can only speculate in the favorable pathophysiological effects behind the good results.

Kåre I. Birkeland