Scientists find a new way insulin-producing cells die
ScienceDaily (Feb. 25, 2011) The death of insulin-producing beta cells in the pancreas is a core defect in diabetes. Scientists in Italy and Texas now have discovered a new way that these cells die — by toxic imbalance of a molecule secreted by other pancreatic cells.
“Our study shows that neighboring cells called alpha cells can behave like adversaries for beta cells. This was an unexpected finding,” stated Franco Folli, M.D., Ph.D., professor of medicine/diabetes at The University of Texas Health Science Center at San Antonio. He is co-lead author on the study with Carla Perego, Ph.D., assistant professor of physiology at the University of Milan.
Balance needed to control sugars
Alpha and beta cells are grouped in areas of the pancreas called the islets of Langerhans. Alpha cells make glucagon, the hormone that raises blood sugar during fasting. In the same environment the beta cells make insulin, the hormone that lowers sugars after a meal. Imbalance ultimately leads to diabetes.
“We found that glutamate, a major signaling molecule in the brain and pancreas, is secreted together with glucagon by alpha cells and affects beta cell integrity,” Dr. Folli said. “In a situation where there is an imbalance toward more alpha cells and fewer beta cells, as in Type 1 and Type 2 diabetes, this could result in further beta cell destruction.”
Glutamate toxicity is a new mechanism of beta cell destruction not previously known, Drs. Perego and Folli said. It has not been typically thought that alpha cells could themselves be a cause of beta cell damage, they said.
The study also found a protection for beta cells, namely, a protein called GLT1 that controls glutamate levels outside the beta cells. “GLT1 is like a thermostat controlling the microenvironment of beta cells with respect to glutamate concentration,” Dr. Perego said.
A diagnostic test for glutamate toxicity in the islets of Langerhans is being developed by the authors, Dr. Folli said. Eventually an intervention to slow the process could follow.
Glutamate poisoning is a new candidate mechanism for beta cell destruction in diabetes. Others are high glucose, buildup of a protein called amyloid, and free fatty acids, which are found in patients with type 2 diabetes.
“The vicious cycle in diabetes is that there are several substances that have been shown, also by us, to be toxic to beta cells,” Dr. Folli said. “And now we have found a new one, glutamate.”
The Journal of Biological Chemistry published the study on-line this week. The work of Dr. Perego is supported by a allow from the Italian Ministry of University and Research. Dr. Folli’s work is supported by the National Institutes of Health.
The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Texas Health Science Center at San Antonio, via EurekAlert!, a service of AAAS.
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
source : www.sciencedaily.com
Related News:
- Immune System: How memory B cells stay ‘in class’ to fight different infections
- Major source of cells’ defense against oxidative stress identified
- Treatment of ischemic heart failure with bone marrow cells does not show improvement for certain heart function measures
- Scientists reprogram cancer cells with low doses of epigenetic drugs
- Teaching fat cells to burn calories: New target against obesity involves brown fat
- Diagnostic tool: Polymer film loaded with antibodies can capture tumor cells
- Molecular path from internal clock to cells controlling rest and activity revealed
- Key to immune cell’s ‘internal guidance’ system discovered
- Blacks urged to donate blood, stem cells
- Brain glia cells increase their DNA content to preserve vital blood-brain barrier
Details :
Submited at Saturday, February 26th, 2011 at 7:00 am on Health by arrisa
Comment RSS 2.0 - leave a comment - trackback