Research
This world-class research initiative from the developer of the Edmonton Protocol has the potential to cure diabetes by developing personalized stem-cell based therapies.
One of the major issues with islet transplantation is that close to half of the islets being transplanted are lost within the first few days post-transplant.
Two important discoveries have added direction and excitement to the research program established by Dr. Jean Buteau.
Dr Patrick MacDonald and his team at the Alberta Diabetes Institute IsletCore have made a very important breakthrough in type 2 diabetes. They have identified a new pathway that controls insulin production from pancreatic islet cells. This pathway acts as the ‘dimmer switch’ to determine how much insulin comes out once these cells are ‘turned on’. Scientists have been trying to solve the mystery of the ‘dimmer switch’ for over 20 years. They have found that this dimmer switch is broken in the cells of type 2 diabetics but can be fixed so that diabetic cells work the same as healthy cells. The ability to restore and fix the dimmer switch in islet cells has been proven on a molecular level but the there will be a challenge to translate these findings into clinical use. The Alberta Diabetes Foundation has a 7 year, $100,000 commitment with Dr MacDonald to support his research in this field of study and Dr MacDonald believes the findings show a important new way forward.
This world-class research initiative from the developer of the Edmonton Protocol has the potential to cure diabetes by developing personalized stem-cell based therapies.
One of the major issues with islet transplantation is that close to half of the islets being transplanted are lost within the first few days post-transplant.
Dr. Peter Senior
Director, Alberta Diabetes Institute
Dr. Charles A. Allard Chair in Diabetes Research
2021 Summer Studentships
STUDENT: Ryan Fung ADI SUPERVISOR: Doug Klein AWARD: $6,000 Metabolic syndrome is a cluster of common risk factors such as high blood pressure, high blood sugar, lipid problems, and large waist circumference that makes individuals more susceptible to chronic conditions such as heart disease and diabetes. Approximately 20% of Canadian adults have metabolic syndrome. However, with lifestyle changes to diet and exercise, the progression of metabolic syndrome can be reduced or reversed in some cases. The purpose of this project is to evaluate the effectiveness of digital metabolic rehabilitation in treating metabolic syndrome through a mixed methods design using quantitative and qualitative data. We predict that the virtual delivery of the metabolic rehabilitation program which incorporates online healthcare team sessions, online resources, and wearable health technology will be effective in improving health outcomes while also empowering patients to make meaningful changes to their lifestyle habits.
STUDENT: Jessica Logan ADI SUPERVISOR: Jane Yardley AWARD: $6,000 Post-menopausal women with type 1 diabetes are at higher risk of heart disease, muscle loss, and bone density loss than women without diabetes, leading to an increased risk of frailty. Existing evidence suggests that resistance exercise (RE) reduces these risks, however, it can also increase instability of blood glucose levels in people with type 1 diabetes. This pilot study will test the efficacy and safety of two different RE protocols for post-menopausal women with type 1 diabetes, comparing acute changes in blood glucose levels during exercise, and for 24 hours after exercise using continuous glucose monitoring. The goal of this research is to collect data that can be used to build an optimal resistance exercise program that is both safe and effective for women with type 1 diabetes. Researchers developing the artificial pancreas may also use these data to create age and sex-specific glucose management algorithms.
STUDENT: Yashvi Patel ADI SUPERVISOR: Sue Tsai AWARD: $6,000 Type 1 diabetes (T1D) is an autoimmune disease characterized by T cell attack on insulin-producing beta cells in the pancreas. IgA deficiency is linked to increased susceptibility of developing T1D. Our project aims to understand the mechanistic link betweenIgA-mediated mucosal immunity using an IgA-deficient non-obese-diabetic (NOD) mouse model. Weekly monitoring of abnormal urine glucose will be done to determine when the mice become diabetic. We will use flow cytometry-based immunological assays to mark and count beta-cell-specific lymphocytes in both groups to see what effect IgA deficiency has on autoreactive T cell populations. Mucosal immune responses will also be tracked. Fecal samples will be tested to see if IgA deficiency affects gut microbiota. We expect to gain new insights into how IgA deficiency impacts autoimmune attack of pancreatic beta cells. We anticipate that IgA deficiency may do so through impairing gut homeostasis, mucus barrier function, and disturbing the microbiota of the gut.