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Professor Thornalley said, "It is an honor to have contributed to this pioneering research, which is making a vital contribution to the study of diabetes and to our evolving understanding of the disease. The research team also benefited from the integration of QBRI into our diabetes research center, which is now leading to a deeper understanding of diabetes through our innovative research, which is also an integral part of the study. "
According to researchers at the University of Warwick and the current QBRI, a mechanism in cells that line the blood vessels and helps treat glucose, becomes uncontrolled in diabetic patients and could be related to the formation of blood clots and inflammation.
Dr Omar El-Agnaf, Executive Director of QBRI, said: "Faced with the growing prevalence of diabetes in Qatar and the region, the QBRI is committed to seeking new approaches to address this challenge. major health. In addition, we believe that our efforts can be significantly enhanced through strategic collaborations and that ongoing diabetes research conducted with a leading research university such as the University of Warwick will help us discover information. important with global relevance. "
The researchers examined the impact of normal and elevated glucose levels on human endothelial cells, which form the lining of our blood vessels. By increasing the glucose concentration in the culture medium, the researchers modeled the effects of hyperglycemia on human endothelial cells – a condition in which an individual's blood glucose level is abnormally high and generally caused by diabetes.
Dr. Naila Rabbani, of Warwick School of Medicine, said, "The mechanisms of organ sensitivity to damage caused by high glucose levels in diabetes are still poorly understood and an urgent improvement in the treatment of diabetic complication is necessary. Our study is a step forward in understanding these mechanisms.
"Our research has identified a likely key step, the increase of hexokinase-2 (HK2), in initiating the development of blood vessel lesions in hyperglycemia related to vascular complications of diabetes, such as kidney, nerve damage in the arms and legs, and the increased risk of heart disease – the leading cause of premature death in diabetes. It is important to note that we have shown how a new type of treatment, Glo1 inducer, can correct this problem and deserves to be taken into account in the search for better treatments for diabetes complications. "
The initial study confirmed that glucose metabolism in endothelial cells was increased at high glucose concentrations. They showed for the first time that this occurred because HK2 degraded more slowly in high glucose concentration and thus metabolized more glucose than normal. An increase in glucose metabolism is the motor of metabolic dysfunction of endothelial cells in hyperglycemia pattern.
The QBRI Diabetes Research Center encourages innovative research on type 1 and type 2 diabetes and related metabolic disorders. The main objective of the center is to acquire fundamental knowledge and to improve understanding of the social, molecular and genetic causes of the disease. These efforts will pave the way for the identification of therapeutic targets and the development of new therapies and treatment modalities for this devastating disease worldwide.
About Hamad Bin Khalifa University
Innovate today, shaping tomorrow
The Hamad Bin Khalifa University (HBKU), a member of the Qatar Foundation for Education, Science and Community Development (QF), was founded in 2010 as a research-intensive university that acts as a catalyst for profound change in Qatar and the region. overall impact. Located at Education City, HBKU is committed to strengthening and developing human capabilities through a rewarding academic experience, an innovative ecosystem and unique partnerships. HBKU provides multidisciplinary undergraduate and graduate programs at its colleges and provides research and research opportunities at its institutes and centers. For more information on HBKU, visit www.hbku.edu.qa.
© Press Release 2019
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