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.
Study of seniors finds physical activity, good
dietary habits, not smoking and light alcohol use lowers diabetes risk
by 82%; four in five new cases attributable to not having these low-risk
factors.
"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