Conferences archive > 2008 > SPEAKERS & ABSTRACTS

Barbara Corkey

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.

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