Lead Investigator
Jonathan Cohen, Ph.D. is a human geneticist who, with his scientific collaborator Helen Hobbs, has identified and characterized several key genes and sequence variants contributing to disorders of lipid metabolism and coronary heart disease in humans.
Associate Investigators
Fred Dunn, M.D. is an endocrinologist with significant experience in academics and in the pharmaceutical industry. He has expertise in the design and implementation of clinical trials.
Abhimanyu Garg, M.D. is an endocrinologist and a world authority on the clinical characterization and treatment of lipodystrophy. Dr. Garg discovered two genetic defects causing congenital generalized lipodystrophy and pioneered the use of leptin to treat the severe metabolic complications of this disorder.
Scott Grundy, M.D., Ph.D. is a member of the Institute of Medicine and Director of the Center for Human Nutrition. Dr. Grundy has played a central role in defining the metabolic effects of statins. He is the chair of the National Cholesterol Education Panel, which establishes treatment guidelines for hyperlipidemias.
Helen Hobbs, M.D. is a member of the Institute of Medicine and a Howard Hughes Medical Institute Investigator who discovered ABCG5 and ABCG8, two membrane proteins that mediate cholesterol secretion into bile, and that mutations in ARH produce an autosomal recessive form of severe hypercholesterolemia in humans. She also is the Director of the Reynolds Center at UTSW, which performed the Dallas Heart Study.
Edward Livingston, M.D. is the Director of Gastroenterology/Endocrinology and Bariatric Surgery at UTSW. He has performed studies to define the effectiveness of bariatric surgery for the treatment of obesity.
Gloria Vega, Ph.D. is an expert in the in vivo metabolism of lipoproteins who developed methods to quantify plasma apoB-containing lipoproteins (VLDL, IDL, LDL) and to define the metabolic consequences of drugs used to treat components of the metabolic syndrome.
Andrew Zinn, M.D., Ph.D. is a human geneticist who discovered that mutations in single-minded 1 (SIM1), a protein expressed in the hypothalamus, causes early onset obesity in humans.