报 告 人： Joseph A. Baur, University of Pennsylvania , US
报告题目：“Functional consequences of manipulating NAD in skeletal muscle”
报告时间：2016年11月15日（星期二）上午10:00
报告地点：南京医科大学学海楼B214
Dr. Baur obtained his PhD degree in 2003 from the UT Southwestern Medical Center at Dallas, TX (TX, USA) where he demonstrated the existence of telomere position effect in human cells, this shortening of telomeres can relieve transcription silencing of adjacent genes. He then did his post-doc at Harvard Medical School (Boston, USA) where he identified resveratrol, a small polyphenol that has many biological activities, including activation of sirtuin enzymes, has potent anti-diabetic effects in mice. These studies have contributed to the rationale for many ongoing clinical trials, with an emerging consensus that resveratrol has mild, but beneficial effects in type II diabetics.
He obtained K99/R00 Pathway to Independence Award and New Scholar Award, Ellison Medical Foundation and started his own lab in 2008 as a young investigator in the Institute for Diabetes, Obesity, and Metabolism at School of Medicine in University of Pennsylvania.
His group focuses on elucidating the molecular mechanisms by which dietary restriction (DR) exerts beneficial effects on longevity and metabolism in mammals. One area of interest is the role of changes in nicotinamide adenine dinucleotide (NAD)-metabolism in mediating downstream consequences of DR, including modulation of the activity of sirtuin enzymes. They have characterized strains of mice that overexpress or lack Nampt, resulting in increased or decreased NAD levels in muscle, and have developed extensive methodology for measuring metabolites and related changes in physiology. They are also investigating the possibility that modulation of sirtuin activity, via NAD or small molecule activators such as resveratrol, can improve outcomes for acute stresses, with a particular focus on mitochondrial function in the liver and kidneys during septic shock. A second major focus is on understanding the mechanism of action for rapamycin, an inhibitor of the nutrient-sensing mTOR complexes. They have shown that rapamycin extends life at least in part via inhibition of mTORC1, but also causes detrimental side effects including hepatic insulin resistance via an off-target effect on mTORC2. Their broad goal is to identify molecular mechanisms of DR that are amenable to nutritional or pharmacological manipulation and can be translated into therapies to prevent or treat age-related diseases in humans.