Chicago - 10:00 AM - 11:00 AM
The Department of Biochemistry and Molecular Genetics welcomes you to attend a seminar by faculty candidate Clara Peek, PhD, Research Assistant Professor of Medicine (Endocrinology).
The circadian clock maintains energy constancy by anticipating changes in nutrient availability that occur throughout the daily fasting/feeding cycle. Genetic studies demonstrate that clock genes expressed in different tissues exert distinct and often opposing effects on metabolic physiology at different times of day. Indeed, while clock disruption in pancreas results in postprandial hyperglycemia, clock ablation in liver causes fasting hypoglycemia, however the molecular bases for these abnormalities are not well understood. As a postdoctoral fellow, I helped to discover that the circadian clock controls mitochondrial metabolism via rhythmic production of the metabolic cofactor NAD+, activity of the mitochondrial protein deacetylase SIRT3, and oxidative metabolism in liver. Since skeletal muscle is especially dependent upon oxidative metabolism, and because myopathy is a prominent feature of circadian gene disruption in mice, I was next prompted to examine clock control of fuel metabolism in skeletal muscle, culminating in my most recent discovery of a novel link between circadian clocks and the oxygen- and nutrient-responsive HIF pathway. These studies have led to my present hypothesis that clock-HIF interactions in skeletal muscle are critical for normal muscle physiology and are impaired during circadian disruption.