Barbara E. Corkey, PhD: What We Think We Know about Diabetes that We Don’t Really Know

Dr. Barbara E. Corkey talks about the huge amount of misinformation on the internet regarding substances that may or not cause diabetes. She points out that most of what we know is actually based on correlation rather than solid evidence and cites the example of the U.S. government’s decision to advise a low-fat diet to combat obesity which hasn’t been successful. However, this advice is still being given.

More videos with Dr. Corkey:

Introduction: The Unknown Causes of Diabetes and Obesity
What Environmental Substances May Cause Diabetes?
Why Food and Packaging Industry Should Collaborate More Closely with Researchers
What We Think We Know about Diabetes that We Don’t Really Know
Current Strategies to Combat Obesity Not Working

Barbara E. Corkey, Ph.D., Professor of Medicine, is the Director of the Obesity Research Center (ORC) at the Boston University School of Medicine. Within the ORC basic science environment, Dr. Corkey’s laboratory focuses on the metabolic regulation of signal transduction and energy metabolism and fuel partitioning in fat cells, fuel-stimulated insulin secretion by the pancreatic ß-cell, and cytokine signaling in human fibroblasts from patients with inborn errors of fatty acid oxidation and Type 1 diabetes. The main questions in the Corkey laboratory concern how fuels regulate insulin secretion and how the fat cell determines whether to store or burn fat. The researchers seek to answer these questions by studying the fuel-induced signals that modulate secretion, electrical activity, metabolism and gene expression. Recent discoveries include a putative role for reactive oxygen species in insulin secretion, digital calcium signaling in pancreatic ß-cells and a role for inhibition of the respiratory chain in regulating fat storage in adipocytes. The main tools used in the laboratory include measurement of intracellular ions such as Ca2+ and H+, plasma and mitochondrial membrane potential, oxygen consumption, the signaling consequences of cellular energy state, the influence of ROS and fatty acids on protein kinases and the role of fatty acids and long chain fatty acyl CoA on signal transduction.