General fitness, health and nutrition · Public discussion

Prevented autoimmune disease

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15 May 2007
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  1. Glucosamine-like supplement inhibits multiple sclerosis, type 1
    diabetes

    Metabolic therapy shows promise for treating autoimmune diseases, UC
    Irvine study finds

    Irvine, Calif., May 14, 2007
    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 normalized 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.

    Ani Grigorian, Sung-Uk Lee, Wenqiang Tian, I-Ju Chen and Guoyan Gao of
    UC Irvine and Richard Mendelsohn and James W. Dennis of the Samuel
    Lunenfeld Research Institute in Toronto participated in the study,
    which was funded by the National Institutes of Health, the National
    Multiple Sclerosis Society, the Juvenile Diabetes Research Foundation,
    the Wadsworth Foundation and the Canadian Institutes for Health
    Research.

    About the University of California, Irvine: The University of
    California, Irvine is a top-ranked university dedicated to research,
    scholarship and community service. Founded in 1965, UCI is among the
    fastest-growing University of California campuses, with more than
    25,000 undergraduate and graduate students and about 1,800 faculty
    members. The second-largest employer in dynamic Orange County, UCI
    contributes an annual economic impact of $3.7 billion. For more UCI
    news, visit www.today.uci.edu.

    Television: UCI has a broadcast studio available for live or taped
    interviews. For more information, visit www.today.uci.edu/broadcast.

    News Radio: UCI maintains on campus an ISDN line for conducting
    interviews with its faculty and experts. The use of this line is
    available free-of-charge to radio news programs/stations who wish to
    interview UCI faculty and experts. Use of the ISDN line is subject to
    availability and approval by the university.

    ------------------------------------------------------------------

    Source: Thomas Jefferson University Released: Mon 28-Nov-2005,
    15:40 ET

    Printer-friendly Version

    Over-the-Counter Arthritis Drug Might Help Against MS
    Libraries
    Medical News Keywords
    MS, ARTHRITIS
    Contact Information

    Available for logged-in reporters only
    Description

    Glucosamine, the over-the counter natural product that has been
    touted
    to help with joint and cartilage problems associated with arthritis,
    may also provide some relief to individuals with multiple sclerosis
    (MS).

    Newswise - Glucosamine, the over-the counter natural product that has
    been touted to help with joint and cartilage problems associated with
    arthritis, may also provide some relief to individuals with multiple
    sclerosis (MS), a degenerative, nervous system disease with no known
    cure.

    Using a mouse model of MS, neurologists at Jefferson Medical College
    found that doses of glucosamine similar to those taken for
    osteoarthritis dramatically delayed the onset of symptoms and
    improved
    the animals' ability to move and walk.

    The scientists, led by A. M. Rostami, M.D., Ph.D., professor and
    chair
    of the Department of Neurology at Jefferson Medical College of Thomas
    Jefferson University and the Jefferson Hospital for Neuroscience in
    Philadelphia, and Guang-Xian Zhang, M.D., Ph.D., assistant professor
    of
    neurology at Jefferson Medical College, say the treatment's
    anti-inflammatory effects may be useful in conjunction with more
    mainstream therapies such as beta-interferon in helping patients with
    MS to delay or perhaps stave off some of the debilitating effects of
    the disease. They report their findings in the December 1, 2005 of
    The
    Journal of Immunology.

    "It would be fantastic if glucosamine works in humans because we have
    a product that has a long track record for safety, and most
    importantly, can be given orally," says Dr. Rostami, who is also
    director of the Neuroimmunology Laboratory in the Department of
    Neurology at Jefferson Medical College. He notes that current
    treatments for MS are given by injection. He hopes to test
    glucosamine
    in clinical trials in the near future.

    MS, one of the most common neurological diseases affecting young
    adults, is thought to be an autoimmune disease (in which the body
    attacks its own tissue) affecting the central nervous system (CNS).
    In
    MS, the myelin coating of nerve fibers becomes inflamed and scarred.
    As
    a result, "messages" cannot be sent through the nervous system.

    Dr. Rostami and his group used an animal model of MS called
    experimental autoimmune encephalomyelitis (EAE), which mimics the
    human
    disease, to investigate glucosamine's potential immune
    system-suppressing properties. Such animals gradually develop the
    disease.

    In the studies, some of the mice received glucosamine, while others
    did
    not.

    They gave glucosamine to the mice three ways: orally,
    intraperitoneally
    and intravenously. They also tested the drug in one set of animals
    before the onset of symptoms, and in another group at the time the
    animals began to show symptoms.

    In each case, the researchers showed they could significantly prolong
    the onset of disease. That is, those animals that got glucosamine
    took
    longer to get ill and once they became ill, the disease was much less
    severe. It was just as effective when given early in the disease or
    when the animals became sick.

    They examined the animals' spinal cords and found less inflammation
    and "demyelination" in those that were given glucosamine.

    "As a therapy, it might be used in combination with other proven
    treatments, such as beta-interferon and copaxone," says Dr. Rostami.

    The research team has some ideas of how glucosamine exerts its
    effects.
    According to Dr. Rostami, EAE and MS are caused by abnormal responses
    from the immune system's T cells. There are two types: TH1, which
    promotes inflammation, and TH2, which is anti-inflammatory. "We've
    shown the glucosamine modulates the immune response by producing more
    TH2 responses, suppressing brain inflammation," he says. "At the
    same time, it suppresses TH1 response."

    The researchers currently are testing the effectiveness of
    combinations
    of glucosamine and standard drugs for MS in the same mouse model to
    look for adverse effects. They are also trying to find out if
    glucosamine can suppress the relapses in the relapsing/remitting form
    of the disease.

    Relapsing/remitting is the most common form of MS. Patients
    experience
    clearly defined "flare-ups," acute episodes in which neurological
    functions worsen, followed by partial or complete recovery periods.

    Over 400,000 Americans acknowledge having MS; however, many
    neurologists believe that nearly one million Americans are living
    with
    MS in the United States today. Symptoms can include fatigue, loss of
    coordination, muscle weakness, numbness, inability to walk or use
    hands
    and arms, pain, vision problems, slurred speech, decline in the
    ability
    to think and reason, and bladder/bowel dysfunction.

    ---------------------------------------------------------------------------­-----

    © 2005 Newswise. All Rights Reserved.

    ---------------------------------------------------------------------------­-----

    <<snip>>
    The results indicated that these complexes could be used in
    eliminating
    the excess iron(III) in living organisms.
    <<snip>>

    J Inorg Biochem. 2002 Apr 28;89(3-4):212-8. Related Articles, Links

    Aqueous and solid complexes of iron(III) with hyaluronic acid.
    Potentiometric
    titrations and infrared spectroscopy studies.

    Merce AL, Marques Carrera LC, Santos Romanholi LK, Lobo Recio MA.

    Departamento de Quimica, Universidade Federal do Parana, CP 19081,
    Centro
    Politecnico, Curitiba, 81531-990, Brazil. [email hidden]

    The coordination of iron(III) ion to hyaluronic acid (Hyal) in
    aqueous
    solutions and solid state was accomplished by potentiometric
    titrations
    and
    infrared spectroscopy. The potentiometric titration studies provided
    the
    binding constants for the complexes found in the systems and the
    speciation of
    these species according to the variation of pH values. The complexes
    found
    presented a complexing ability through both the chelating moieties of
    Hyal (via
    the N-glucosamine and D-glucoronic acid), showing no special
    preference
    for
    either one while in solid state, but when in aqueous solution the
    complexation
    via the N-glucosamine moiety was the preferred, forming two complexed
    species,
    ML and ML(2) (log K(ML)=8.2 and log K(ML2)=7.9). The presence of a
    mu-oxo
    complex via the D-glucoronic acid was also detected in both aqueous
    (log K=6.7)
    and solid states via the N-glucosamine and D-glucoronic acid
    simultaneously
    linked to two Hyal chains. A structure for this latter complex was
    suggested.
    The results indicated that these complexes could be used in
    eliminating
    the
    excess iron(III) in living organisms.

    PMID: 12062125 [PubMed - indexed for MEDLINE]

    --------------------------------------------------------------------------

    ------

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