biotech
N-Acetylglucosamine Inhibits Multiple Sclerosis, Type 1 Diabetes
Filed in archive Drugs, Vaccines and Therapeutics , Food and Agriculture by ruth on May 21, 2007
N-Acetylglucosamine Inhibits Multiple Sclerosis, Type 1 Diabetes
A glucosamine-like dietary supplement, N-acetylglucosamine (GlcNAc), has been found to suppress the damaging autoimmune response observed in multiple sclerosis and type 1 diabetes mellitus.
In studies on mice, Dr. Michael Demetriou and colleagues with the UC Irvine Center for Immunology found that N-acetylglucosamine (GlcNAc), which is similar but more effective than the widely available glucosamine, inhibited the growth and function of abnormal T-cells that incorrectly direct the immune system to attack specific tissues in the body, such as brain myelin in MS and insulin-producing cells of the pancreas in diabetes.

Together with a recent study on the use of GlcNAc in the treatment of treatment-resistant autoimmune inflammatory bowel disease, these findings point to the use of metabolic therapy using dietary supplements such as GlcNAc for treating autoimmune diseases.

More details from UC Irvine.


Permalink: N-Acetylglucosamine Inhibits Multiple Sclerosis, Type 1 Diabetes
Tags: multiple+sclerosis  diabetes  acetylglucosamine  dietary+supplement  autoimmune+disease  biotech  biotech+ 
Trackback: http://publish.creative-weblogging.com/publish/mt-tb.pl/70739
img Addthis img Ask img Blinklist img del.icio.us img Digg img Fark img Facebook img Google img Lycos img Ma.gnolia Add this page to Mister Wong Mr Wong img Netscape img Netvousz img Newsvine img Reddit img StumbleUpon img Slashdot img Tailrank img Technorati img Wink img Yahoo

Vote for N-Acetylglucosamine Inhibits Multiple Sclerosis, Type 1 Diabetes:

  • Currently 9.00/10
  • 1
  • 2
  • 3
  • 4
  • 5
  • 6
  • 7
  • 8
  • 9
  • 10
Rating: 9.00 out of 11 vote(s) cast.
 
Subscribe
Share It
RSSrss
See all blog subscribe options
Google google
What is RSS?
Yahoo! yahoo
Addthis Subscribe using any feed reader!
Bloglines Bloglines
Newsletter

TwitterFollow us on Twitter!