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Einstein Scientist Receives Prestigious International Award for His Research In Diabetes

October 3, 2003 -- (BRONX, NY) -- Michael Brownlee, M.D., of the Albert Einstein College of Medicine of Yeshiva University, has received the 2003 Claude Bernard Medalfrom the European Association for the Study of Diabetes (EASD) for his outstanding contributions to the understanding of diabetic complications. The Medal is the highest scientific honor given by the EASD and is recognized as one of the world's most prestigious awards for diabetes research. 

As this year's recipient, Dr. Brownlee delivered the Claude Bernard Lecture at the combined EASD/International Diabetes Federation meeting in Paris on August 28, 2003. "Brownlee is a household word in the field of diabetic complications," said EASD President Phillipe Halban in his introduction of Dr. Brownlee. "What makes him remarkable is that he has transformed an entire discipline with his landmark studies. His work in the field of molecular complications has been unusually inventive."

Dr. Brownlee's most recent major contribution to complications research is the 
discovery of a mechanism through which high blood sugar (hyperglycemia) causes damage to small blood vessels in the eye and kidney. Over the past 35 years, four seemingly independent major mechanisms of hyperglycemia-induced damage have been discovered: polyol pathway activation, advanced glycation endproduct (AGE) formation, protein kinase C (PKC) activation, and hexosamine pathway activation. 

Dr. Brownlee's research has established that these biochemical pathways all arise from a single hyperglycemia-induced process-they are initiated by overproduction of toxic "free radicals" produced by the cells' energy factories, the mitochondria. He also has demonstrated that normalizing the levels of these excess free radicals inhibits the pathways through which cell damage occurs, and that all of these pathways can be activated, even in the presence of normal glucose levels, simply by using molecular genetic techniques to shut down the key enzyme that high glucose turns off.

In his Claude Bernard Lecture, Dr. Brownlee described how complications researchers have pieced together the multiple causes of damage, explained the biochemical basis for the unified hypothesis, and listed several potential agents for blocking the damage.

In research described in the March 2003 issue of the journal Nature Medicine, the drug, benfotiamine, a synthetic derivative of the dietary supplement thiamine (vitamin B1), was found to block all major pathways of hyperglycemia damage, and most importantly, blocked formation of structural lesions in the retinas of long-term diabetic animals. Benfotiamine has been prescribed for more than a decade in Germany for nerve conditions and is generally regarded as being safe without harmful side effects. Dr. Brownlee is currently testing benfotiamine in human clinical trials, in a study sponsored by the Juvenile Diabetes Research Foundation.

To conclude his presentation, Dr. Brownlee underscored the devastating toll of diabetes-related complications by showing a brief video clip about Paul Abercrombie, who began developing diabetic complications at age 18 and passed away just four years later. Dr. Brownlee, who has had type 1 diabetes since age 8, told the audience "It is my most cherished dream and hope that the new science I have told you about in my lecture will soon mean that type 1 diabetics and their families will never again have to worry about the possibility of a future like Paul's."

Dr. Brownlee holds the Anita and Jack Saltz Chair of Diabetes Research at the Albert Einstein College of Medicine, where he is a Professor of Medicine and Pathology. He also is Co-Director of the Diabetes Research Center there. He is a past member of the Juvenile Diabetes Research Foundation's Medical Science Advisory Board and the past Chairman of the American Diabetes Association's (ADA's) Council on Complications. Ten years ago, Dr. Brownlee received another of the world's most prestigious awards for diabetes research, the ADA's Out

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