Sulfurophane and Myostatin Inhibition - AnabolicMinds.com

Sulfurophane and Myostatin Inhibition

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    Sulfurophane and Myostatin Inhibition


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    genetics. 2012 Dec 1;7(12):1379-90. doi: 10.4161/epi.22609. Epub 2012 Oct 23.Sulforaphane causes a major epigenetic repression of myostatin in porcine satellite cells.

    Fan H, Zhang R, Tesfaye D, Tholen E, Looft C, Hölker M, Schellander K, Cinar MU.
    Source

    Institute of Animal Science; Animal Breeding and Husbandry Group; University of Bonn; Bonn, Germany.

    Abstract

    Satellite cells function as skeletal muscle stem cells to support postnatal muscle growth and regeneration following injury or disease. There is great promise for the improvement of muscle performance in livestock and for the therapy of muscle pathologies in humans by the targeting of myostatin (MSTN) in this cell population. Human diet contains many histone deacetylase (HDAC) inhibitors, such as the bioactive component sulforaphane (SFN), whose epigenetic effects on MSTN gene in satellite cells are unknown. Therefore, we aimed to investigate the epigenetic influences of SFN on the MSTN gene in satellite cells. The present work provides the first evidence, which is distinct from the effects of trichostatin A (TSA), that SFN supplementation in vitro not only acts as a HDAC inhibitor but also as a DNA methyltransferase (DNMT) inhibitor in porcine satellite cells. Compared with TSA and 5-aza-2'-deoxycytidine (5-aza-dC), SFN treatment significantly represses MSTN expression, accompanied by strongly attenuated expression of negative feedback inhibitors of the MSTN signaling pathway. miRNAs targeting MSTN are not implicated in posttranscriptional regulation of MSTN. Nevertheless, a weakly enriched myoblast determination (MyoD) protein associated with diminished histone acetylation in the MyoD binding site located in the MSTN promoter region may contribute to the transcriptional repression of MSTN by SFN. These findings reveal a new mode of epigenetic repression of MSTN by the bioactive compound SFN. This novel pharmacological, biological activity of SFN in satellite cells may thus allow for the development of novel approaches to weaken the MSTN signaling pathway, both for therapies of human skeletal muscle disorders and for livestock production improvement.


    PMID: 23092945 [PubMed - in process] PMCID: PMC3528693 [Available on 2013/12/1]


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    Saw this posted on another forum. There are some sulfurophane supps out there but according to my research they are innefective see here
    Sulforaphane works as a potent catalyst to boost Phase 2 enzymes in the body. These detoxification enzymes trigger ongoing antioxidant action for at least 72 hours. As a result, the indirect antioxidant activity of sulforaphane lasts significantly longer than that of direct antioxidants, such as vitamins C, E and beta carotene, although it also boosts the regeneration of the active forms of these vitamins. Furthermore, three-day-old sprouts have a much higher concentration of glucoraphanin than the average mature broccoli (73 mg v. 11 mg per serving, respectively), which means one ounce of broccoli sprouts contains as much glucoraphanin as over 1.25 pounds (20 ounces) of average market-stage broccoli. However, the range of glucoraphanin varies considerably with the variety of broccoli grown, so that in market broccoli, there is at least a 15-fold range of glucoraphanin (Brown et al., J.Am. Hort. Soc. 2002). The highest concentration of glucoraphanin is found in the seed. Eating the raw, unsprouted seed could provide high amounts of sulforaphane, but seeds also contain the antimetabolite erucic acid, which is metabolized during sprouting, so eating seeds is not recommended.
    Prepared extracts of either broccoli seeds or broccoli sprouts typically lose their myrosinase activity. As a result, the content of glucoraphanin may remain, but without the presence of the myrosinase, the ability to convert the bioactive sulforaphane has been lost. Based on some limited evidence from animal studies, the colonic microflora may have some myrosinase-like activity. One study suggests this may provide no more than 8% conversion.[7] A human study[8] showed there is such large interindividual variability in the population of colonic microflora in humans, such that any conversion to sulforaphane is not only limited, but also unpredictable. Other researchers have similarly found there is limited sulforaphane bioavailability in broccoli sprouts preparations in which the myrosinase has been destroyed.
    So cannot use supplemental forms because they won't work.

    My research revealed that sulfurophane which is found in broccoli and broccoli sprouts has a host of health
    benefits outside the myostatin inhibition. It is found in Broccoli sprouts at up to 50x the amount in the same weight of broccoli. Broccoli Sprouts cost 4 bucks for 4 ounces at the local heath food store so... screw that... I've started growing my own to get it in its effective form. There is approximately 2 mg of Sulurophane in a pound of broccoli, (once its constituents are activated by chewing) which means there would be 40-100 mg's in a pound of sprouts.

    My question is, how many pounds of sprouts would I need to eat to consume enough sulfurophane to test the theory of Myostatin inhibition? i.e. more muscle growth
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    Interesting topic. In for more answers on this
    Will start growing broccoli sprouts right away until dosing is found out

    Or maybe we will see a sulfuraphane powder/cap product from PN?
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    Regarding your dosing question I found this:

    Sulforaphane appears to be well absorbed, as numerous studies in humans following the consumption of broccoli have noted increased urinary metabolites of Sulforaphane.[11][12] In humans, bioavailability of sulforaphane appears to be 74% and primarily absorbed in the jejunum.[13]
    In rats, an oral dose of 50umol (8.8mg; which is 58-73mg/kg) appears in the blood within 1 hour and peaks 4 hours after consumption, reaching 20uM; this does is accompanied by a 2.2 hour half-life and reaching close to baseline levels 12 hours after consumption.[14]

    The enzyme CYP2A6 (responsible for metabolism of Nicotine) may be regulated via Sulforaphane's ability to induce Nrf2, which has been induced up to 1.4fold control levels with 10uM Sulforaphane,[26] and CYP2A6 has been noted to be increased after 6 days of broccoli sprout consumption at 500g per day by a variable 1.4-5.5 fold increase.[27] Variances may be due to differing activity of the Antioxidant Response Element (ARE1) that Nrf2 activation works via.[26]
    6. Interactions with Skeletal Muscle

    6.1. Myostatin

    Possibly secondary to its ability to act as a Histone Deacetylase Inhibitor, Sulforaphane may repress Myostatin transcription and attenuate negative feedback on Myostain suppression in porcine satellite cells.[46] It has been noted elsewhere in liver fibrosis pathology that neither NQO1 and HO-1 (downstream of Nrf2) but Nrf2 itself disrupted signalling from TGF-β to Smad proteins, via inhibiting nuclear accumulation of Smad3;[47] one of the proteins which mediate the actions of Myostatin in the nucleus.[48] However, application of these mechanisms to satellite cells may not be valid as Sulforaphane appears to regulate TGF-β/Smad signalling differentially depending on the cellular conditions.[49][9]
    The aforementioned study in pigs noted that both Sulforphane and the reference drug 5-aza-2′-deoxycytidine suppressed Myostatin, but not trichostatin A (another Histone Deacetylase Inhibitor).[46] Sulforaphane at 5, 10, and 15uM concentration (achieveable with oral intake) failed to increase Follistatin concentrations (natural antagonist to Myostatin) but increases in Smad7 and Smurf1 mRNA was noted, with most significance at 5uM.[46] miRNAs that increase Myostatin signalling did not appear to be downregulated, with only suppression in miR-29a and miR-29b.[46]
    One study in skeletal muscle satellite cells noting an attenuation of Myostatin signalling (an anabolic event), possibly due to interactions with Sulforaphane's HDAC or Nrf2 inhibitor actions; practical relevance for muscle hypertrophy unclear
    Interestingly, this study noted a significant reduction in MyoD mRNA levels at 10uM concentration (5uM not tested) in these porcine satellite cells, coupled with diminished binding to the Myostatin promoter via hypoacetylation of the binding site.[46]

    Dunno how much it helps you but it's a start
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    Quote Originally Posted by truthornothin View Post
    See Below




    Saw this posted on another forum. There are some sulfurophane supps out there but according to my research they are innefective see here

    So cannot use supplemental forms because they won't work.

    My research revealed that sulfurophane which is found in broccoli and broccoli sprouts has a host of health
    benefits outside the myostatin inhibition. It is found in Broccoli sprouts at up to 50x the amount in the same weight of broccoli. Broccoli Sprouts cost 4 bucks for 4 ounces at the local heath food store so... screw that... I've started growing my own to get it in its effective form. There is approximately 2 mg of Sulurophane in a pound of broccoli, (once its constituents are activated by chewing) which means there would be 40-100 mg's in a pound of sprouts.

    My question is, how many pounds of sprouts would I need to eat to consume enough sulfurophane to test the theory of Myostatin inhibition? i.e. more muscle growth

    sounds like you have delved into the research more than i have. are you bad at math or something?
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    Quote Originally Posted by Patrick Arnold View Post
    sounds like you have delved into the research more than i have. are you bad at math or something?
    Actually yes I am, but not that bad, I can only get hold of the abstract and I don't see the dosages that they used, I know you are able to get the full studies and thought you might help a brother out
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    Quote Originally Posted by truthornothin View Post
    Actually yes I am, but not that bad, I can only get hold of the abstract and I don't see the dosages that they used, I know you are able to get the full studies and thought you might help a brother out
    i get them thru beejis usually. gimme a link to the study you want
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    I have a hard time keeping track of all these different sulfur based compounds. Between Methylsulfonylmethane (MSM), DMSO, and all the sulfur containing amino acids (Taurine, NAC, etc.).

    Would this possibly be the same for other sulfur based compounds like say, Garlic? I mean is it the sulfur that is the active ingredient here? I remember reading somewhere that the reason glucosamine sulfate shows better results than glucosamine hcl is because maybe sulfur is the thing doing the work in the first place.
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    here's what I read: metabolismjournal.com/article/S0026-0495(01)83589-7/abstract

    put www in front of that
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    Quote Originally Posted by GigaPaladin View Post
    I have a hard time keeping track of all these different sulfur based compounds. Between Methylsulfonylmethane (MSM), DMSO, and all the sulfur containing amino acids (Taurine, NAC, etc.).

    Would this possibly be the same for other sulfur based compounds like say, Garlic? I mean is it the sulfur that is the active ingredient here? I remember reading somewhere that the reason glucosamine sulfate shows better results than glucosamine hcl is because maybe sulfur is the thing doing the work in the first place.

    it is not just the sulfur atom on any of these
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