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Harvard Scientists Move Closer to Correcting Cellular Defects That Lead to Diabetes

Report says the G6PD protein, which produces essential antioxidant NAPDH, could prevent the death of pancreatic beta cells, the root cause of diabetes

Jan. 4, 2010 - In a new research report, scientists say they are coming closer to correcting the root cause of diabetes through the identification of a protein (G6PD) and its antioxidant product (NAPDH) that both prevent the death and promote the growth of cells which produce and release insulin in the pancreas (beta cells).

This new discovery published online in the FASEB Journal (http://www.fasebj.org) could change the perception and treatment of diabetes, according to the publication's news release.

 

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Read the latest news on Senior Health & Medicine

 

"Abnormally high levels of oxidants are thought to be a major cause of diabetes and the complications of diabetes, as well as many other diseases," said Robert C. Stanton, M.D., co-author of the study, from Joslin Diabetes Center in Boston, an affiliate of the Harvard Medical School.

"By understanding the specific defects in processes that either produce too many oxidants or not enough antioxidants, a new era of highly specific, targeted treatments will emerge that very effectively treat or possibly prevent many of these diseases."

To make this discovery, Stanton and colleagues studied beta cells from humans and mice to determine the effects of increasing sugar on the cells, the G6PD protein, and NADPH antioxidant.

Using biochemical and molecular biology techniques, researchers measured levels of various chemicals, proteins and markers of both cell growth and death. Results showed that increasing the level of sugar causes a decrease in NADPH and increased beta cell death.

Additionally, tweaking the level of NADPH higher prevented the negative effects of increased sugar. Increasing the activity of G6PD rescued the beta cells from cell death, leading researchers to conclude that treatments that directly prevent G6PD decrease or promote G6PD increases could hold great promise in treating diabetes.

"Even before the 'omic revolution, the cause and cure of diabetes have long been sought," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal.

"This research discovery, which identifies a key enzyme that regulates oxidation and pancreatic cell death, brings us closer than ever to getting at the root of diabetes."

Source:

The FASEB Journal (http://www.fasebj.org) is published by the Federation of the American Societies for Experimental Biology (FASEB). The journal has been recognized by the Special Libraries Association as one of the top 100 most influential biomedical journals of the past century and is the most cited biology journal worldwide according to the Institute for Scientific Information. FASEB comprises 22 nonprofit societies with more than 80,000 members, making it the largest coalition of biomedical research associations in the United States. FASEB advances health and welfare by promoting progress and education in biological and biomedical sciences through service to its member societies and collaborative advocacy.

Details: Zhaoyun Zhang, Chong Wee Liew, Diane E. Handy, Yingyi Zhang, Jane A. Leopold, Ji Hu, Lili Guo, Rohit N. Kulkarni, Joseph Loscalzo, and Robert C. Stanton. High glucose inhibits glucose-6-phosphate dehydrogenase, leading to increased oxidative stress and -cell apoptosis
FASEB J. doi:10.1096/fj.09-136572 ; http://www.fasebj.org/cgi/content/abstract/fj.09-136572v1

>> Federation of American Societies for Experimental Biology

 

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