My third day in San Francisco starts with a session on “The Resilient Beta Cell in Type 2 Diabetes”. Emerging research is indicating that not all beta cells are equal and that some have very different levels of activity. Professor Jim Johnston from the University of British Columbia in Canada explains that individual beta bells transition in and out of states of extreme insulin production but that these periods render the cells more fragile and susceptible to death which may have relevance not just to type 2 diabetes but to type 1 diabetes as interplay between the environmental beta cell stressors like diet or infection and a genetic predisposition could lead of endoplasmic reticular stress and apoptosis or, in the case or type 1 diabetes, a predisposition to T-cell mediated destruction of the beta cell.
The following session by Professor Brigid Gregg from the University of Michigan focusses on early life influence on pancreatic beta cell mass and function. Thirty years on from the seminal work of David Barker in which he proposed that restricted intrauterine growth, low birth weight and premature birth all have a causal relationship with high blood pressure and coronary heart disease in additional to an increased risk of developing type 2 diabetes in later life, she reflects on the effects of overnutrition or undernutrition and of metformin on maternal health in an animal model. Although there is no difference in beta cell morphology postnatally, islets do have increased insulin content following exposure to a high fat diet. Programmed offspring outcomes include weight gain, increased adiposity and increased metabolic disease whilst metformin exposed pups have decreased circulating insulin and weigh significantly less than non-metformin exposed pups. She highlights the importance of maternal health during and after pregnancy.
The EASD e-Learning platform already offers a course in gestational diabetes (GDM) which has been created to introduce you to the epidemiology and current screening controversies of GDM. Treatment, management and the long-term follow-up of women with GDM are also covered. Please click here to access this course.
Peripheral neuropathy and diabetic foot disease contribute significantly to the global diabetes mortality and morbidity figures. My next session is on “Common Practices That Do Not Make Sense – Dilemmas in Diabetic Foot Management” started with an assessment of sagittal force versus shear force wounds and the skeletal reconstruction and tendon rebalancing corrections like exostectomy, arthrodesis and tendon lengthening and release with the emphasis on offloading for diabetic foot ulcer healing and recurrence prevention. The importance of diagnosing diabetic foot infection clinically and not based on findings from wound-surface swabs was also made. Because of the inexorable increase in multidrug resistant organisms, the speakers stressed tissue biopsy and cultures as alternative procedures because of a 90% specificity and 95% accuracy for predicting wound closure. Debridement was also focussed on from the biological kinds using leeches or maggots, through enzymatic and autolytic to mechanical using irrigation and hydrotherapy.
In autumn 2019, the EASD e-Learning team will be launching a suite of modules about the diabetic foot built with experts from Ireland, the UK, Germany and Qatar. If you would like to be notified when these modules launch, please click here to register your interest.
And, finally, on a busy Day 3, the results of the REWIND trial were announced. This multicentre, randomised, double-blind, placebo-controlled trial was done at 371 sites in 24 countries. Men and women aged at least 50 years with type 2 diabetes who had either a previous cardiovascular event or cardiovascular risk factors were randomly assigned (1:1) to either weekly subcutaneous injection of dulaglutide (1·5 mg) or placebo. The results showed that, in middle aged and older men and women, similar to people with type 2 diabetes in the general population, with a broad range of glycaemic control and high use of at least one cardiovascular (CV) protective drug adding dulaglutide safely reduced CV outcomes for more than five years. Similar benefits were observed in men and women and the outcomes irrespective of body mass index or glycaemic control as measured by HbA1c. This led the investigators to conclude that the addition of dulaglutide could be considered for both primary and secondary CV prevention in middle aged patients with type 2 diabetes and CV risk factors.
The slides from this presentation were made available directly after the presentation and can be accessed here and two papers of the trial results were published simultaneously (Gerstein et al; Gerstein et al).
The EASD e-Learning platform already features a suite of modules on the action of SGLT inhibitors in type 2 diabetes as well as in type 1 diabetes. If you are interested in finding out more about drug actions and advice on how and when to use them, please click here and leave feedback for the team. We’d be interested to hear from you as to what you would like to see on the platform!