Barbara E. Corkey is Vice-Chair for Research and Professor of Medicine and Biochemistry in the Department of Medicine at Boston University School of Medicine, where she is also Director of the Obesity Research Center of Boston Medical Center and the Principal Investigator of the multi-institutional NIH-funded Boston-Obesity/Nutrition Reseach Center. She is was Chair of the Board of AdipoGenix, a start-up drug company that she co-founded to develop drugs to treat obesity. She just completed a term as Editor-in-Chief of the journal Obesity. She has chaired the program committee for the national annual meeting of the American Diabetes Association, served on the National Peer Review Oversight Committee for the American Heart Association and served on review committees of the NIH and the Juvenile Diabetes Foundation.
Professor Corkey received her PhD in 1981 from the University of Pennsylvania, Department of Biochemistry and Biophysics for studies focusing on branched chain amino acid metabolism. She has published over 100 manuscripts and been invited to speak at numerous national and international institutions and symposia.
The main questions in the Corkey laboratory concern how fuels regulate insulin secretion and how the fat cel determines whether to store or burn fat. We seek to answer these questions by studying the fuel- induced signals that modulate secretion, electrical activity, metabolism and gene expression. Recent discoveries include a role for reactive oxygen species in insulin secretion, digital calcium signaling in
pancreatic ß-cel s 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 intracel ular ions such as Ca2+ and H+, plasma and mitochondrial membrane potential, oxygen consumption, the signaling consequences of cel ular energy state, the influence of fatty acids on protein kinases and the role of fatty acids and long chain fatty acyl CoA on signal transduction. Work is supported by three NIH RO1 grants and done in colaboration with scientists at Boston University, Tufts University, the Karolinska Institute, the Universities
of Montreal and Pennsylvania and the CIIT Centers for Health Research.
Professor Corkey is also an avid painter, grandmother and wine connoisseur.
Obesity and Diabetes: Excess Food or Toxic Environment
The increased prevalence of obesity in the US population began about 1980 and is continuing worldwide. By 2015 1.5 billion people ofthe predicted 8 billion world population,(19%),willbe obese. WHOestimates thatby then non-communicable diseases willbe the main causes ofmorbidity and mortality globally.
The resource burden of chronic disease engendered by obesity is now added to that of malnutrition and infection in developing countries. The complications of obesity related diabetes, stroke and heart disease are seen at lower body weight in certain Asian and Hispanic populations and are seen with weight gain in abdominal fat depots. Treatment of these three diseases is a great burden to all societies. For example, China expects to spend $556 billion on diabetes, heart disease and stroke during the ten years between 2005 and 2015. In developed nations it is now predicted that decreased life expectancy will be the result of increasing obesity. Even more alarming, treatment is largely unsuccessful and dedicated therapists who have placed patients on “diet plans” espoused in the last forty years have usually been frustrated, with failure ultimately blamed on lack ofpatientcompliance,notscientific ignorance.
Epidemiologic studies have provided some correlations with obesity including: psychotropic medication use, home temperature, mother’s age at first birth, smoking, time spent awake, being Hispanic in the USA, being age 35 to 55, increased food intake, decreased activity, fast food availability, and global warming. Additional changes in the past half century include: vitamin / mineral contentof fruits and vegetables, body composition of food animals and the introduction of thousands of food additives into our food supply. The causes of obesity may be associated with some or many ofthese changes.
Justas itis criticalto continue to investigate these correlations,italso is crucialto investigate the fuel::::energy equations at the physiologic, biochemical and molecular levels. For a long time, increased fat was seen as a cosmetic issue by governments. Recent knowledge shows adipose tissue to be a very dynamic actor in energy balance. Simple models that equated fat accumulation with overeating alone have not held up. Scientific studies of normal, weight stable individuals who have been enlisted to either restricted diet or forced overeating show a return, up or down, to their baseline weight, rapidly and spontaneously. This yo-yo effect is also seen in the vast majority of obese dieters and favors the presence of yet other factors in body weight balance. The fat cell number in the body is largely determined in childhood; for those in whom this is excessive, neither aging nor weight loss in later years changes this number. To treat malnutrition in children with solutions thatcause obesity may yieldchronic disease in childhood and adulthood.
Neither obesity nor malnutrition will abate until sufficient understanding of the metabolic engine that we all are has been achieved. When pathways, genetics, and cell signaling are understood in a holistic way, then rational choices of treatments can be offered to the earth’s people. As we have learned in the past decades, one mustbe astute to avoid implying causation when our data show only a correlation.
Future science must improve our scientific and technological understanding of nutrition with consideration for the economic and ethicalimplications ofpoor choices.