Alcoholic fatty liver / lecithin / phosphatidylcholine

Discussion in 'Food and nutrition' started by [email protected], Jan 27, 2005.

  1. <<snip>>
    The endotoxin-stimulated tumor necrosis factor-alpha release is
    decreased by dilinoleoylphosphatidylcholine, the active
    phosphatidylcholine (PC) species of polyenylphosphatidylcholine (PPC).
    <<snip>>

    Alcohol. 2004 Aug;34(1):9-19. Related Articles, Links


    Alcoholic fatty liver: its pathogenesis and mechanism of progression to
    inflammation and fibrosis.

    Lieber CS.

    Bronx Veterans Affairs Medical Center, Bronx, NY 10468, USA; Mount
    Sinai School of Medicine, New York, NY 10029, USA.

    Liver disease in the alcoholic is due not only to malnutrition but also
    to ethanol's hepatotoxicity linked to its metabolism by means of the
    alcohol dehydrogenase and cytochrome P450 2E1 (CYP2E1) pathways and the
    resulting production of toxic acetaldehyde. In addition, alcohol
    dehydrogenase-mediated ethanol metabolism generates the reduced form of
    nicotinamide adenine dinucleotide (NADH), which promotes steatosis by
    stimulating the synthesis of fatty acids and opposing their oxidation.
    Steatosis is also promoted by excess dietary lipids and can be
    attenuated by their replacement with medium-chain triglycerides.
    Through reduction of pyruvate, elevated NADH also increases lactate,
    which stimulates collagen synthesis in myofibroblasts. Furthermore,
    CYP2E1 activity is inducible by its substrates, not only ethanol but
    also fatty acids. Their excess and metabolism by means of this pathway
    generate release of free radicals, which cause oxidative stress, with
    peroxidation of lipids and membrane damage, including altered enzyme
    activities. Products of lipid peroxidation such as 4-hydroxynonenal
    stimulate collagen generation and fibrosis, which are further increased
    through diminished feedback inhibition of collagen synthesis because
    acetaldehyde forms adducts with the carboxyl-terminal propeptide of
    procollagen in hepatic stellate cells. Acetaldehyde is also toxic to
    the mitochondria, and it aggravates their oxidative stress by binding
    to reduced glutathione and promoting its leakage. Oxidative stress and
    associated cellular injury promote inflammation, which is aggravated by
    increased production of the proinflammatory cytokine tumor necrosis
    factor-alpha in the Kupffer cells. These are activated by induction of
    their CYP2E1 as well as by endotoxin. The endotoxin-stimulated tumor
    necrosis factor-alpha release is decreased by
    dilinoleoylphosphatidylcholine, the active phosphatidylcholine (PC)
    species of polyenylphosphatidylcholine (PPC). Moreover, defense
    mechanisms provided by peroxisome proliferator-activated receptor alpha
    and omega fatty acid oxidation are readily overwhelmed, particularly in
    female rats and also in women who have low hepatic induction of fatty
    acid-binding protein (L-FABPc). Accordingly, the intracellular
    concentration of free fatty acids may become high enough to injure
    membranes, thereby contributing to necrosis, inflammation, and
    progression to fibrosis and cirrhosis. Eventually, hepatic
    S-adenosylmethionine and PCs become depleted in the alcoholic, with
    impairment of their multiple cellular functions, which can be restored
    by PC replenishment. Thus, prevention and therapy opposing the
    development of steatosis and its progression to more severe injury can
    be achieved by a multifactorial approach: control of alcohol
    consumption, avoidance of obesity and of excess dietary long-chain
    fatty acids, or their replacement with medium-chain fatty acids, and
    replenishment of S-adenosylmethionine and PCs by using PPC. Progress in
    the understanding of the pathogenesis of alcoholic fatty liver and its
    progression to inflammation and fibrosis has resulted in prospects for
    their better prevention and treatment.

    PMID: 15670660 [PubMed - in process]

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

    Who loves ya.
    Tom

    Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
    Man Is A Herbivore!
    http://pages.ivillage.com/ironjustice/manisaherbivore
    DEAD PEOPLE WALKING
    http://pages.ivillage.com/ironjustice/deadpeoplewalking
     
    Tags:


  2. [email protected] wrote:

    ---------- Forwarded message ----------
    From: [email protected]
    Date: 17 Jan 2005 15:11:02 -0800
    Subject: Re: Liver steatosis /serum iron / transferrin saturation /
    ferritin

    Now .. john .. when markd .. attacks me .. it is the 'frog' .. humping
    ... me ..eh ..

    So what does that mean .. YOU .. do ..?

    Eh .. pussssiiiieeee ..

    Eh ..

    Heh .. heh ..

    Who loves ya.
    Tom

    Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
    Man Is A Herbivore!
    http://pages.ivillage.com/ironjustice/manisaherbivore
    DEAD PEOPLE WALKING
    http://pages.ivillage.com/ironjustice/deadpeoplewalking
     
Loading...