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1900 links for PBM studies

Discussion in 'Redox Rx' started by Jack Kruse, Dec 2, 2021.

  1. Since we know -> The liver is a key player in the role of lipid metabolism.

    ULK1 promotes mitophagy via phosphorylation and stabilization of BNip3
    UNC51-like kinase-1 (ULK1) is the catalytic component of the autophagy pre-initiation complex that stimulates autophagy via phosphorylation of ATG14, BECLN1 and other autophagy proteins.

    ULK1 promotes BNIP3 protein stability by preventing its proteasomal degradation

    Diagram summarizing the model for how ULK1 promotes BNIP3-dependent mitophagy—by both blocking its proteasomal turnover and phosphorylating BNIP3 to promote interaction with LC3B.​
    Ok so, we know BNip3 is a main player in the regulation of lipid metabolism in the liver and that ULK1 promote mitophagy stabilizing BNip3.

    Question -> What can we do to improve these mitochondrial functions?

    There maybe two potential answers:
    • Phytochemicals
    • Photobiomodulation
    Let's start with phytochemicals. Phytochemicals derived from natural plants are often used to prevent and/or treat metabolic disorders due to their unique therapeutic properties and safety (Bacanli et al., 2019). Plentiful medicinal and non-medicinal natural plants have been used to treat diseases from time immemorial in the world on account of the accessibility and low cost. Studies have shown that phytochemicals such as akebia saponin D, quercetin, cyanidin-3-O-glucoside, corilagin, notoginsenoside R1, scutellarin, salvianolic acid B, resveratrol and curcumin show protective effects against metabolic diseases, and their plant origins, effects and molecular mechanisms on metabolic diseases are provided in Table 1 ->





    Phytochemical activates mitophagy to treat metabolic disorders. Phytochemical activates PINK1-Parkin-dependent mitophagy and BNIP3/NIX-dependent mitophagy to treat metabolic disorders. In PINK1-Parkin-dependent mitophagy, PINK1 phosphorylates Ser65 in the ubiquitin and ubiquitin-like domain of Parkin and further facilitates its localization from the cytosol to the outer mitochondrial membrane of dysfunctional mitochondria. Moreover, Parkin can further promote the ubiquitination of MFN1, MFN2, TOM20 and VDAC, which can be identified by autophagy receptors p62 and then bind to LC3 positive autophagosomes to promote dysfunctional mitochondria to be captured by autophagosomes. Additionally, BNIP3 and NIX are easier to bind to Bcl-2 and Bcl-XL than Beclin1, which causes the release of Beclin-1 from Beclin1-Bcl-2-Bcl-XL complexes and subsequently induces mitophagy.


    Ok so, we got a list of phytochemicals which can help with liver fatty acid metabolism.

    Question: What treatments would a quantum clinician use to enhance lipid metabolism in the liver?

    Since you are a Gold Member, please consider asking @Jack Kruse during the June 2022 - Quantum Biologic PowWow this weekend. Let me know if you are willing. We could post his response as a reply to your thread.
    Last edited: Jun 17, 2022
    JanSz likes this.
  2. JanSz

    JanSz Gold

    I have already signed up for June 2022 PowWow.

    Possibly @Jack Kruse will see the question here and have time to answer it.
  3. He has never read from these questions before.
    He only answers questions asked during the PowWow.
    JanSz likes this.
  4. JanSz

    JanSz Gold

    Let's see what happens.
    I did asked the question,
    I submitted it while
    signing up for PowWow second time
    it was past the time allowed for submitting questions

    John Schumacher likes this.

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