RxPG News Feed for RxPG News

Medical Research Health Special Topics World
 Asian Health
 Food & Nutrition
 Men's Health
 Mental Health
 Occupational Health
 Public Health
 Sleep Hygiene
 Women's Health
 Canada Healthcare
 China Healthcare
 India Healthcare
 New Zealand
 South Africa
 World Healthcare
   Latest Research
 Alternative Medicine
 Clinical Trials
   Insulin Resistance
 Infectious Diseases
 Sports Medicine
   Medical News
 Awards & Prizes
   Special Topics
 Odd Medical News

Last Updated: Oct 11, 2012 - 10:22:56 PM
Research Article
NIDDM Channel

subscribe to NIDDM newsletter
Latest Research : Endocrinology : Diabetes : NIDDM

   EMAIL   |   PRINT
Data support role for adult spleen cells in regeneration of beta cells

Nov 24, 2006 - 10:42:30 PM , Reviewed by: Sanjukta Acharya
"This data from the NIH and the earlier studies have added significantly to the understanding of how diabetes may be reversed,"

[RxPG] New data published in the Nov. 24 issue of Science provide further support for a protocol to reverse type 1 diabetes in mice and new evidence that adult precursor cells from the spleen can contribute to the regeneration of beta cells. In 2001 and 2003, researchers at Massachusetts General Hospital (MGH) demonstrated the efficacy of a protocol to reverse of type 1 diabetes in diabetic mice. Three studies from other institutions published in the March 24, 2006 issue of Science confirmed that the MGH-developed protocol can reverse the underlying disease but were inconclusive on the role of spleen cells in the recovery of insulin-producing pancreatic islets. The new data from a study performed at the National Institutes of Health (NIH), published as a technical comment, provides additional confirmation of the ability to reverse type 1 diabetes and on the role of the spleen cells in islet regeneration.

"This data from the NIH and the earlier studies have added significantly to the understanding of how diabetes may be reversed," says Denise Faustman, MD, PhD, director of the Immunobiology Laboratory at Massachusetts General Hospital, primary author of the 2001 and 2003 studies and co-corresponding author of the current report. "It is still early, but it appears that there are multiple potential sources for regenerating islets. As a research community we should pursue all avenues. We're excited to see what will happen in humans."

In the 2001 and 2003 studies, Faustman and colleagues treated end-stage nonobese diabetic (NOD) mice with Freund's complete adjuvant, a substance that suppresses the activity of the immune cells that destroy islets in type 1 diabetes. They also introduced donor spleen cells to retrain the immune system not to attack islets and found that the protocol not only halted the immune destruction caused by diabetes but also allowed the insulin-producing pancreatic islet cells to regenerate. Evidence indicated that the spleen cells were the source of at least some of the regenerated islet cell and hastened the restoration of blood sugar levels.

The direct contribution of spleen cells to islet recovery, first described in the 2003 study, is confirmed in the current work. NIH researchers used cell lineage tracking in the form of Y-chromosomal fluorescence in situ hybridization (FISH), in combination with insulin staining, to follow the fate of male spleen cells transplanted into female recipients. The female mice that received male donor cells consistently showed Y-chromosome-positive insulin-producing islet cells, indicating that the introduced spleen cells contribute to islet recovery. The current study also showed that the degree of spleen cell contribution is influenced by mouse age at the start of treatment. Spleen cells appear to contribute to islet recovery more in mice who are older and with more advanced diabetes compared with younger mice with less advanced diabetes, in which regeneration of remaining islets may be the dominant mechanism.

Publication: March 24, 2006 issue of Science
On the web: www.mgh.harvard.edu 

Funding information and declaration of competing interests: The research to support the new data was conducted at the NIH laboratory of Eva Mezey, MD, PhD, co-corresponding author of the report. It was funded by the Sjogren's Syndrome Foundation, National Institutes of Health/NIDCR intramural program, Canadian Institutes of Health Research and Canada Research Chair. The three studies published in March 2006 were supported by the Juvenile Diabetes Research Foundation. Faustman's research at Massachusetts General Hospital has been supported by The Iacocca Foundation, which is also supporting a clinical trial program based on her research.

Advertise in this space for $10 per month. Contact us today.

Related NIDDM News
Data support role for adult spleen cells in regeneration of beta cells
Researchers reveal mechanisms behind Thiazolidinediones in type 2 diabetes
High-fat diet supresses GnT-4a activity to cause type 2 diabetes
Low blood glucose levels may complicate gastric bypass surgery
Muraglitazar found to increase adverse cardiovascular events
Insulin's role in blocking release of energy
TORC2 - Key regulator of blood glucose levels discovered
Panel Recommends Muraglitazar for the Treatment of Type 2 Diabetes
Persons at risk for type 2 diabetes have lower rate of cellular energy production
Sirt1 protein enhances the secretion of Insulin

Subscribe to NIDDM Newsletter

Enter your email address:

 Additional information about the news article
Massachusetts General Hospital, established in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of nearly $500 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, transplantation biology and photomedicine. MGH and Brigham and Women's Hospital are founding members of Partners HealthCare System, a Boston-based integrated health care delivery system.
For any corrections of factual information, to contact the editors or to send any medical news or health news press releases, use feedback form

Top of Page

Contact us

RxPG Online



    Full Text RSS

© All rights reserved by RxPG Medical Solutions Private Limited (India)