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200.000 euro to diabetes research
Published 29 May 2017
Four researchers have been awarded grants from The Bo and Kerstin Hjelt Diabetes Foundation. The grant consists of Euro 50 000 each and are aiming towards better treatments and prevention of type 2-diabetes.
Improved life expectancy and quality of people with diabetes
Diabetes affects millions of patients around the world. The two main types of the disease, type 1 and type 2, are both characterized by progressive beta-cell death and can lead to insulin deficiency. Chronic high blood levels, polydipsia, polyuria, weight loss and ketoacidosis are among the clinical manifestations of insulin deficiency. This condition leaves patients dependent on insulin treatment for life. Unfortunately, insulin replacement is not sufficient to reproduce the control of metabolic homeostasis seen in healthy subjects. In fact, patients receiving quotidian insulin injections are prone to accumulation of lipids in tissues and are at constant risk of hypoglycemia. This is due to insulin’s lipogenic and glycaemia fast lowering actions. Thus, better interventions are urgently needed. The studies proposed in this project are based on strong preliminary data uncovering a molecular component with unpredicted role against both type 1 and type 2 diabetes. The grant generously offered by the Bo and Kerstin Hjelt Diabetes Foundation will be used to characterize this unexpected anti-diabetic effect and investigate the mechanism of action. Results from our study have the potential to unravel a novel therapeutic target with the ultimate goal to improve life expectancy and quality of the millions affected by diabetes.
Project: Life without insulin: Testing the anti-diabetic role of a candidate involved in inflammation
Sanda Ljubicic and Giorgio Ramadori, University of Geneva
Identification and prevention of diabetic kidney disease
Diabetic kidney disease affects almost 30 percent of diabetic patients and is a prime reason for kidney function loss. High blood glucose may contribute to diabetic kidney disease progression, and several studies including my previous publications have shown that diabetic kidney disease development may involve glucose-triggered epigenetic changes, which will be the focus of this project.
Epigenetic changes may occur via modifications on the histone proteins, around which the DNA strand winds and packs into chromosome structure. Based on our previous research, we suggest that glucose may modify histones on various locations, leading to changes in DNA packaging structure, and consequently affects gene activity that contributes to diabetic kidney disease development. Here we will make detailed analysis on histone modifications in blood from diabetic patients with Diabetic kidney disease, and associate these changes to diabetic kidney disease risk.
This study will hopefully contribute to better understanding of diabetic kidney disease pathogenesis. The epigenetic markers in blood identified in this project may be used as predictive biomarkers for diabetic kidney disease. Once validated, patients can be screened by simple blood tests for presence of these markers without invasive biopsy procedures. Patients at high diabetic kidney disease risk can be thereby identified to allow intensified therapy to prevent diabetic kidney disease.
Project: New Epigenetic Targets for Diabetic Kidney Disease Prediction
Yang De Marinis, PhD, Diabetes and Endocrinology, Lund University Diabetes Centre, Sweden
Why high blood sugar damages insulin producing cells
The information that will emanate from this project would have great impact on the prevention of T2D in view of the years of dysregulated blood glucose control preceding the outbreak of the disease.
A hallmark of type 2 diabetes is decreased insulin secretion and a loss of functional beta-cells, leading to dysregulation of blood glucose control. The elevated average blood glucose concentrations consequently exert harmful effects on the insulin secreting beta-cells, so called glucotoxicity. Since beta-cell mitochondria play a central role in the coupling of glucose metabolism to insulin secretion, their dysfunction has been implicated in the defective hormone release in type 2-diabetes. A key regulator of mitochondrial function is the voltage-dependent anion channel 1 (VDAC1), a multi-functional protein located on the outer mitochondrial membrane (OMM) mediating the fluxes of nucleotides and metabolites across the OMM. Changes in the VDAC1 or VDAC2 function have been related to impaired mitochondrial metabolism and apoptosis. The present project aims to identify the mechanisms underlying pancreatic beta-cell dysfunction during episodes of glucotoxicity and to dissect the complex signaling network involved in hyperglycemia-induced beta-cell dysfunction in human islets and also in relevant animal models of type 2 diabetes.
Project: Blocking aberrant cell surface mitochondrial VDAC1 is associated with restoration of insulin secretion in diabetes
Albert Salehi, University of Lund, Department of Clinical Science, Division Islet Cell Physiology; Malmö, Sweden
New markers and therapeutic targets to prevent cardiovascular events
The risk of dying from cardiovascular disease is increased among individuals with type 2-diabetes. Type 2-diabetes is increasing fast and considering the high risk to suffer from a cardiovascular event it is crucial to increase our knowledge regarding atherosclerosis in type 2-diabetes. Through the identification of biological differences in type 2-diabetes we aim to find markers and therapeutic targets to prevent cardiovascular events.
The risk of suffering from cardiovascular events as myocardial infarction and stroke is increased for individuals with type 2-diabetes. These complications are commonly caused by ruptures of vulnerable atherosclerotic plaques, located in the large arteries. The cause of the increased risk to suffer from a vulnerable plaque rupture among individuals with type 2-diabetes remains unknown.
We recently showed that atherosclerotic plaques from individuals with type 2-diabetes have signs of an impaired arterial tissue repair as a potential cause of the high risk for a plaque rupture.
We aim to identify if the impaired tissue repair might be caused by a defect inflammatory resolution and clearance of dead cells, two important steps in tissue healing and regeneration.
By characterizing the role of these processes in the arterial wall we further aim to assess if they might be possible to trace in blood as biomarkers or by imaging to identify high risk individuals.
Project:”Diabetes associAantderedas vEdassfecldut lar complications caused by impaired efferocytosis, inflammatory resolution and fibrotic tissue repair”