For Immediate Release
Contact: Megan Rowe
(434) 924-5679
meganrowe@virginia.edu
UVA RECEIVES $9 MILLION GRANT FOR DIABETES AND ATHEROSCLEROSIS RESEARCH
Charlottesville, Va. - Recent news reports note that for the first time in history, the world has more obese people than hungry people. Obesity is a leading cause of diabetes and can contribute to the thickening and hardening of arteries (known as atherosclerosis), which in turn can lead to an increased incidence of heart disease.
The University of Virginia Health System is battling these diseases with four distinct projects that look at possible relationships between obesity, diabetes and atherosclerosis. To help UVa's research, the National Heart, Lung, and Blood Institute has renewed a $9.15 million grant to Dr. Jerry Nadler, chief of the UVa Division of Endocrinology and Metabolism.
"It's a wonderful collaborative program that involves both physicians and scientists in the School of Medicine from different departments and divisions," Dr. Nadler said. "The research will help us to better understand the link between obesity, diabetes and heart disease and to ultimately develop new treatments."
Dr. Klaus Ley, a UVa Harrison Medical Teaching Professor of Biomedical Engineering, Professor of Molecular Physiology and Biological physics and director of the Robert M. Berne Cardiovascular Research Center, will be heading one of the four projects, which looks at the role of lymphocytes in atherosclerosis. According to his lab's research, lymphocytes migrate through the wall of the aorta even before atherosclerosis begins. "This suggests that the immune system may play a part in atherosclerosis and how diabetes accelerates it," Dr. Ley said.
The renewal of this grant will let the UVa Division of Endocrinology and Metabolism and the Cardiovascular Research Center (CVRC) continue their important research into which components of diabetes and central obesity - in which the main deposits of body fat are around the abdomen - lead to accelerated rates of blocked arteries and vascular injury. The metabolic syndrome, a dangerous combination of pre-diabetes and heart-disease factors that affects up to 25 percent of the population, is a chief culprit in American illness.
Project 1 - led by Dr. Nadler: Will utilize models of insulin resistance (often a pre-diabetic condition) and diabetes to test the hypothesis that oxidized lipids including those generated by 12/15-lipoxygenase (12/15-LO) play a role in vascular disease and inflammation by activation of particular immune cells. Researchers will study the link between activation of components of the immune system and development of the chronic inflammation leading to atherosclerosis.
Project 2 - led by Dr. Catherine Hedrick, CVRC: Will test the hypothesis that chronic high blood sugar in diabetes decreases macrophage (an immune cell) ABCG1 function and results in increased macrophage foam cell formation in living models. Researchers hypothesize that the reduction in macrophage ABCG1 function increases atherosclerosis in the setting of diabetes.
Project 3 - led by Dr. Coleen McNamara, CVRC : Will explore the important role of vascular smooth muscle cell (VSMC) growth given the importance of this growth in restenosis (return of blood vessel blockages after treatment) following vascular injury in insulin-resistant and diabetic states.
Project 4 - led by Dr. Klaus Ley, CVRC: Will explore the significant hypothesis that lymphocyte (type of white blood cell) trafficking into and out of the walls of large arteries is changed in insulin-resistant states and diabetes and that this process contributes to accelerated atherosclerosis. The project will explore why and how atherosclerosis results in chronic inflammation of blood vessel walls and how insulin resistance and diabetes modified this process.
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