Spring 2017 Biology Seminar Series: Kai Zou
Biology Professor Kellee Siegfried is hosting this week's Seminar Series. She is bringing in guest speaker Dr. Kai Zou from the University of Massachusetts Boston. The title of his talk is "Defective Glucose Metabolism in Severe Obesity: Causes and Interventions." The discussion abstract is as follows:
"Obesity, particularly severe obesity (BMI > 40 kg/m2), is linked with a myriad of metabolic aberrations which contribute to an increased risk for conditions such as cardiovascular disease, and type 2 diabetes. It is evident that altered glucose metabolism is an important cause of insulin resistance and metabolic derangements associated with severe obesity. With insulin stimulation, the fate of glucose is altered in severely obese subjects in a manner that partitions more glucose towards non-oxidized glycolysis (i.e. lactate production) rather than complete oxidation, indicating glucose oxidation is impaired with severe obesity. The skeletal muscle of severely obese individuals displays defects in glucose metabolism along with insulin resistance; these defects are retained in primary human skeletal muscle cell (HSkMC) cultures, a model that has been utilized to study muscle-specific metabolic phenotypes. In addition, by applying radioactive isotope tracer to HSkMCs, along with metabolomics analysis, we found that the impaired glucose oxidation appears to be due to reduced tricarboxylic acid (TCA) cycle flux.
Roux-en-Y gastric bypass (RYGB) surgery is the most commonly performed weight loss surgery for severely obese people. Remarkably, blood lactate concentrations were dramatically reduced within a week after Roux-en-Y (RYGB) surgery and were retained at 3 months after surgery, suggesting RYGB surgery corrects defective glucose oxidation associated with severe obesity. We further determined that the improved glucose metabolism was retained in primary human muscle cells derived from RYGB surgery patients after surgery, indicating RYGB surgery may alter the inherent metabolic profile of skeletal muscle and possibly involve epigenetic alterations. We are currently using human skeletal muscle cell culture and RYGB surgery as models to understand the cellular mechanisms behind the defective glucose metabolism associated with severe obesity and the beneficial effects of RYGB on metabolic profile to identify potential novel targets for development of treatments of severe obesity and type 2 diabetes."
Please note the time difference.
For disability-related accommodations, including dietary accommodations, please visit www.ada.umb.edu two weeks prior to the event.