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    Chi mi da una mano? Importante...

    Allora, mi sono reso conto che nella mia palestra c'è troppa ignoranza. Il bello è che la cultura delle bombe si sta sempre + radicando (mai avvenuto) mentre nessuno sa cosa è l'acido alfa lipoico. Allora, io mi sono messo daccordo con il proprietario e abbiamo deciso che avrei scritto un bell'articolo sull'acido alfa lipoico (e poi anche su altro) con tanto di bibliografia, proprio come la trovate sui classici M&F o flex, ecc....

    Ora ho bisogno di un aiuto: mi serve che mi riportiate tutti gli studi che avete tra le zampe (anche gli studi, non solo la bigliografia, e possibilmente sull'uomo) a riguardo di:

    1- ruolo di antiossidante
    2- ruolo di epatoprotettore
    3- ruolo di insulinomimetico
    4- ruolo di prevenzione nei confronti delle ulcere etanolo-indotte.
    5- ruolo di enhancer delle trasmissioni neuronali

    Sarà costretto a spiegare tutto punto per punto, come agisce l'insulina, cosa sono i recettori, cosa è il glutatione e che ruolo ha, insomma tutto. Poi finito l'articolo, lo piazziamo qui su bodyweb e una copia la appiccico in palestra, con la scritta "realizzato con la collaborazione dei ragazzi del forum di www.bodyweb.it"

    Allora, comincio io, spulciando tra i topic presenti in Scientific Corner (quello di Animal).
    Sono poche le cose che fanno la differenza...

    #2
    1: Free Radic Biol Med 1998 Apr;24(6):1023-39 Related Articles, Books, LinkOut


    Alpha-lipoic acid in liver metabolism and disease.

    Bustamante J, Lodge JK, Marcocci L, Tritschler HJ, Packer L, Rihn BH.

    Department of Molecular and Cell Biology, University of California, Berkeley 94720-3200, USA.

    R-alpha-Lipoic acid is found naturally occurring as a prosthetic group in alpha-keto acid dehydrogenase complexes of the mitochondria, and as such plays a fundamental role in metabolism. Although this has been known for decades, only recently has free supplemented alpha-lipoic acid been found to affect cellular metabolic processes in vitro, as it has the ability to alter the redox status of cells and interact with thiols and other antioxidants. Therefore, it appears that this compound has important therapeutic potential in conditions where oxidative stress is involved. Early case studies with alpha-lipoic acid were performed with little knowledge of the action of alpha-lipoic acid at a cellular level, but with the rationale that because the naturally occurring protein bound form of alpha-lipoic acid has a pivotal role in metabolism, that supplementation may have some beneficial effect. Such studies sought to evaluate the effect of supplemented alpha-lipoic acid, using low doses, on lipid or carbohydrate metabolism, but little or no effect was observed. A common response in these trials was an increase in glucose uptake, but increased plasma levels of pyruvate and lactate were also observed, suggesting that an inhibitory effect on the pyruvate dehydrogenase complex was occurring.
    During the same period, alpha-lipoic acid was also used as a therapeutic agent in a number of conditions relating to liver disease, including alcohol-induced damage, mushroom poisoning, metal intoxification, and CCl4 poisoning.
    Alpha-Lipoic acid supplementation was successful in the treatment for these conditions in many cases. Experimental studies and clinical trials in the last 5 years using high doses of alpha-lipoic acid (600 mg in humans) have provided new and consistent evidence for the therapeutic role of antioxidant alpha-lipoic acid in the treatment of insulin resistance and diabetic polyneuropathy. This new insight should encourage clinicians to use alpha-lipoic acid in diseases affecting liver in which oxidative stress is involved.
    Sono poche le cose che fanno la differenza...

    Commenta


      #3
      1: Acta Gastroenterol Latinoam 1996;26(3):167-71 Related Articles, Books, LinkOut


      Thioctic acid protection against ethanol and indomethacin induced gastric mucosal lesions in rats.

      Gutierrez-Cabano CA, Valenti JL.

      Department of Surgical Pathology II, Faculty of Medical Sciences National University of Rosario, Argentina.

      BACKGROUND/AIMS: The gastric protective effect of thioctic acid, a sulfhydryl compound, against chemically induced mucosal lesions has not been reported. METHODS: Fasted Wistar rats (24 h) were treated (gavage administration) with graded doses of thiotic acid (12.5, 25, 37.5, 50 mg/kg) followed 0.5 h later by the gavage administration of 1 ml 96% ethanol or intraperitoneal administered indomethacin.
      The gastric mucosa was examined grossly and histologically for an evaluation of the lesions. RESULTS: Pretreatment of rats with thiotic acid has shown a significant decline in the mean number, size, incidence and severity of mucosal lesions induced by both ethanol and indomethacin.
      CONCLUSIONS: This is the first evidence that thiotic acid protects the rat gastric mucosa against chemically induced damage. Its is speculated that this finding may prove to be important in the development of improved therapies for the prevention and treatment of gastric ulcers in humans.
      Sono poche le cose che fanno la differenza...

      Commenta


        #4
        6 Am J Physiol 1997 Jul;273(1 Pt 1):E185-91 Differential effects of
        lipoic acid stereoisomers on glucose metabolism in insulin-resistant
        skeletal muscle. Streeper RS, Henriksen EJ, Jacob S, Hokama JY, Fogt
        DL, Tritschler HJ. Department of Physiology, University of Arizona,
        Tucson 85721-0093, USA. The racemic mixture of the antioxidant
        alpha-lipoic acid (ALA) enhances insulin-stimulated glucose metabolism
        in insulin-resistant humans and animals. We determined the individual
        effects of the pure R-(+) and S-(-) enantiomers of ALA on glucose
        metabolism in skeletal muscle of an animal model of insulin
        resistance, hyperinsulinemia, and dyslipidemia: the obese Zucker
        (fa/fa) rat. Obese rats were treated intraperitoneally acutely (100
        mg/kg body wt for 1 h) or chronically [10 days with 30 mg/kg of
        R-(+)-ALA or 50 mg/kg of S-(-)-ALA]. Glucose transport [2-deoxyglucose
        (2-DG) uptake], glycogen synthesis, and glucose oxidation were
        determined in the epitrochlearis muscles in the absence or presence of
        insulin (13.3 nM). Acutely, R-(+)-ALA increased insulin-mediated
        2-DG-uptake by 64% (P < 0.05), whereas S-(-)-ALA had no significant
        effect. Although chronic R-(+)-ALA treatment significantly reduced
        plasma insulin (17%) and free fatty acids (FFA; 35%) relative to
        vehicle-treated obese animals, S-(-)-ALA treatment further increased
        insulin (15%) and had no effect on FFA. Insulin-stimulated 2-DG uptake
        was increased by 65% by chronic R-(+)-ALA treatment, whereas S-(-)-ALA
        administration resulted in only a 29% improvement. Chronic R-(+)-ALA
        treatment elicited a 26% increase in insulin-stimulated glycogen
        synthesis and a 33% enhancement of insulin-stimulated glucose
        oxidation. No significant increase in these parameters was observed
        after S-(-)-ALA treatment. Glucose transporter (GLUT-4) protein was
        unchanged after chronic R-(+)-ALA treatment but was reduced to 81 +/-
        6% of obese control with S-(-)-ALA treatment. Therefore, chronic
        parenteral treatment with the antioxidant ALA enhances
        insulin-stimulated glucose transport and non-oxidative and oxidative
        glucose metabolism in insulin-resistant rat skeletal muscle, with the
        R-(+) enantiomer being much more effective than the S-(-) enantiomer.
        PMID: 9252495

        Questo è proprio bello. Praticamente:
        Ratti Zucker obesi, sono stati trattati con r-ala o s-ala per via intraperitoneale, sia acuta che cronica.
        Trasporto di glucosio [2-deoxyglucose
        (2-DG) uptake], sintesi del glicogeno, e ossidazione del glucosio sono stati esaminati nel muscolo epitrochlearis in assenza o presenza di insulina. risultato:

        r-ala: in somministrazione acuta, aumenta l'uptake di glucosio del 64%
        s-ala: piombo

        r-ala: in somministrazione cronica, riduce l'insulina plasmatica del 17% e gli FFA del 35%
        s-ala: aumenta la secrezione di insulina del 15% e non ha effetto sugli FFA.

        r-ala: l'uptake del glucosio insulino-indotto, aumenta del 65% in trattamento cronico;
        s-ala: stesse condizioni, aumenta solo del 29%

        r-ala: cronico, induce un aumento della sintesi del glicogeno insulino-stimolata del 26% e aumenta del 33% l'ossidazione del glucosio insulino-indotta.
        s-ala: piombo completo

        r-ala: piombo
        s-ala la proteina del trasportatore di glucosio si è ridotta dell'81% dopo somministrazione cronica.
        Sono poche le cose che fanno la differenza...

        Commenta

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