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    You are here : Home » MS Research News » New Discoveries » N-acetylglucosamine (GlcNAc) & Glucosamine

    N-acetylglucosamine (GlcNAc) & Glucosamine

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    Dietary supplement suppresses immune attacks in MS

    N-acetylglucosamineA dietary supplement similar to glucosamine appears to suppress the damaging autoimmune response seen in multiple sclerosis (MS) attacks, raising hopes of a new metabolic therapy for autoimmune diseases.

    Researchers from the University of California, Irvine (UCI) in the US found that oral N-acetylglucosamine (GlcNAc) stopped abnormal T-cells from growing and working properly: in people with MS, these abnormal cells incorrectly tell the immune system to destroy the tissue that insulates the nerves. You can read a scientific paper about their study in the 29 September online issue of Journal of Biological Chemistry.

    N-acetylglucosamine (GlcNAc) is similar to but more effective than the widely available glucosamine.

    Senior investigator and neurologist Dr Michael Demetriou is associate professor of neurology and microbiology & molecular genetics at UCI and also associate director of the university's Multiple Sclerosis Research Center. He told the media:

    "This sugar-based supplement corrects a genetic defect that induces cells to attack the body in MS."

    He said this could lead to a metabolic therapy that is very different to current treatments.

    Earlier this year, he and his colleagues discovered that previously unconnected and poorly understood environmental and inherited risk factors for MS work together to add certain sugars to proteins that affect the disease.

    Proteins are the workhorses of cells: and they receive their instructions via complex sugar molecules of various sizes and chemical make-up.

    Recent research has found that changes to these sugars may be involved in what makes immune system T-cells become hyperactive in autoimmune diseases, resulting in a destruction of the tissue that protects the nerve fibers and stops the electrical impulses from leaking out.

    For their study, Demetriou and colleagues used lab mice bred to have an MS-like autoimmune disease. They gave the mice oral GlcNAc and found that those whose legs had become weak from the disease showed a reversion of the progression to paralysis.

    They write in their paper the treatment suppressed T-cell hyperactivity and autoimmune response by increasing sugar modifications to the T-cell proteins:

    "Oral treatment of mice with the sugar N-acetylglucosamine (GlcNAc) enhances N-glycosylation, suppressing inflammatory T cell responses and an MS like disease when initiated after disease onset."

    Recent studies by other researchers have also been looking at the potential of GlcNAc in humans. One reported that of 12 children with with treatment-resistant autoimmune inflammatory bowel disease who were given the supplement for two years, eight showed significant improvement and no serious adverse side effects were observed.

    Demetriou said when you bring these findings together you can see there is potential for using dietary supplements such as GlcNAc as a metabolic therapy for autoimmune diseases.

    He said people are getting excited about this new approach because it uses a novel mechanism to address T-cell function and autoimmunity and target a molecular defect that promotes disease. Moreover, it is readily available and simple.

    But we still need more studies on human volunteers to assess the full potential of such an approach, cautioned Demetriou.

    Although you can get GlcNAc supplements without a prescription, you should consult with your doctor before using it, he added.

    Funds from the National Institutes of Health and the National Multiple Sclerosis Society in the US helped pay for the study.

    Source: Medical News Today © MediLexicon International Ltd 2004-2011 (02/10/11)

    Cell-surface sugar defects may trigger nerve damage in multiple sclerosis patients

    Study also suggests treatment for short-term and long-term damage caused by chronic disease.

    Defects on cell-surface sugars may promote the short-term inflammation and long-term neurodegeneration that occurs in the central nervous system of multiple sclerosis patients, according to University of California, Irvine researchers.

    The findings also suggest that a dietary supplement similar to glucosamine may be useful as an oral therapy to correct these defects and to treat both the short-term and the long-term symptoms of the disease. Study results appear on the online version of the Journal of Biological Chemistry.

    “The findings raise the possibility that these may both be treated by metabolic therapy,” said Dr. Michael Demetriou, an assistant professor of neurology, and microbiology and molecular genetics. “This is particularly important, as therapies are not currently available to treat neurodegeneration in MS.”

    In tests on mice, Demetriou found that genetic deficiencies in a process called protein glycosylation led to a spontaneous disease very similar to MS, including paralysis associated with inflammatory damage to the protective myelin coating on nerve cells and degeneration of axons and neurons. Protein glycosylation refers to the addition of specific sugars to proteins; virtually all cell-surface and secreted proteins have complex sugars attached to them.

    MS is a two-stage disease, with initial attacks of inflammatory demyelination, which damages myelin, followed approximately 10 years later by a slow, progressive neurdegenerative phase marked by loss of axons and nerve cells.

    The irreversible damage to the central nervous system induced by neurodegeneration in MS leads to long term disability, including paralysis, incoordination, dementia and pain, and is not targeted by currently available therapies.

    Demetriou’s findings provide the first genetic model of MS in which both inflammatory demyelination and neurodegeneration arise from defects in a single biological pathway.

    In previous studies, Demetriou found that the dietary supplement N-acetylglucosamine (GlcNAc), which is similar but more effective than the widely available glucosamine, corrected defects in protein glycosylation in cells and inhibited inflammatory demyelination in mice. The new study opens the possibility that metabolic therapy with GlcNAc may also prevent neurodegeneration. Studies in humans are required to assess the potential of this therapy in MS.

    Source: University of California, Irvine (21/09/07)

    Glucosamine-like supplement inhibits multiple sclerosis, type 1 diabetes

    A glucosamine-like dietary supplement has been found to suppress the damaging autoimmune response seen in multiple sclerosis and type 1 diabetes mellitus, according to University of California, Irvine health sciences researchers.

    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. Study results appear on the online version of the Journal of Biological Chemistry.

    “This finding shows the potential of using a dietary supplement to help treat autoimmune diseases,” said Demetriou, an assistant professor of neurology, and microbiology and molecular genetics. “Most importantly, we understand how this sugar-based supplement inhibits the cells that attack the body, making metabolic therapy a rational approach to prevent or treat these debilitating diseases.”

    The UC Irvine study defines how metabolic therapy with the sugar GlcNAc and other related nutrients modifies the growth and autoimmune activitiy of T-cells. Virtually all proteins on the surface of cells, including T-cells, are modified with complex sugars of variable lengths and composition. Recent studies have shown that changes in these sugars are often associated with T-cell hyperactivity and autoimmune disease.

    In mouse models of both MS and type 1 diabetes, Demetriou and colleages found that GlcNAc prevented this hyperactivity and autoimmune response by increasing sugar modifications to the T-cell proteins. This therapy normalised T-cell function and prevented development of paralysis in MS and high blood glucose levels in type 1 diabetes.

    This study comes on the heels of others showing the potential of GlcNAc in humans. One previous clinical study reported that 8 of 12 children with treatment-resistant autoimmune inflammatory bowel disease improved significantly following two years of treatment with GlcNAc. No significant adverse side effects were noted.

    “Together, these findings identify metabolic therapy using dietary supplements such as GlcNAc as potential treatments for autoimmune diseases.” Demetriou said. “Excitement for this treatment strategy stems from the novel mechanism for affecting T-cell function and autoimmunity and the availability and simplicity of its use. However, additional studies in humans will be required to assess the full potential of this therapeutic approach.”

    Autoimmune diseases such as MS and type 1 diabetes mellitus result from poorly understood interactions between inherited genetic risk and environmental exposure. MS results in neurological dysfunction, while uncontrolled blood glucose in type 1 diabetes can lead to damage of multiple organs.

    Source: Huliq Breaking News © Huliq.com 2006 (14/05/07)

    Glucosamine could be used in MS?
    Glucosamine, a natural glucose derivative and an essential component of glycoproteins and proteoglycans, has been safely used to relieve osteoarthritis in humans. Recent studies have shown that glucosamine also possesses immunosuppressive properties.

    Whether this reagent is effective in human multiple sclerosis (MS), an inflammatory demyelination in the CNS, is not yet known.

    The therapeutic effect of glucosamine on experimental autoimmune encephalomyelitis (EAE), an animal model of MS was carried out by scientists at Department of Neurology, Thomas Jefferson University, Philadelphia.

    They demonstrated that oral, i.p., or i.v. administration of glucosamine significantly suppressed acute EAE, with reduced Central Nervous Sysytem inflammation and demyelination.

    As glucosamine is able to effectively suppress acute EAE, has low or absent toxicity, and has been safely used in humans orally, the study suggests a potential use for this drug alone or in combination with other disease-modifying immunotherapies to enhance their efficacy and reduce their doses in MS and possibly other autoimmune disorders.

    Furthermore, because glucosamine functions not simply as an immunosuppressant, but as a mild immunomodulator, administration of glucosamine provides a novel immunoregulatory approach for autoimmune disorders

    Taken from a paper published in The Journal of Immunology, December 2005, vol.175, part 11, pages 7202-7208.(28/11/05)

    © Multiple Sclerosis Resource Centre

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