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Hyperlipidemia Promotes Inflammation

Discussion in 'Ask For Help or Advice' started by redlight, Aug 30, 2016.

  1. redlight

    redlight Member

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  2. raypeatclips

    raypeatclips Member

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    I'll let more knowledgable people weigh in on this, but it seems this is the study in question.

    Triglyceride-Rich Lipoproteins Modulate the Distribution and Extravasation of Ly6C/Gr1low Monocytes

    Something that seems odd. "The mice we studied were treated with a drug that caused them to accumulate extremely high levels of fat in their blood."

    Health risks of saturated fats aggravated by immune response

    I am not sure what the drug is, what if the drug is the thing causing the damage? This effect hasn't happened to the mice in the study by simply eating a diet rich in saturated fat.

    "We think that maintaining a relatively high concentration of saturated fats for example by constantly snacking on cakes, biscuits, and pastries could be causing monocytes to migrate out of the blood and into surrounding tissues.”

    Cakes, biscuits and pastries would predominantly be PUFA, I'd imagine. Misrepresenting saturated fat a bit there.
     
  3. Giraffe

    Giraffe Member

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    Don't inject tensides! :ss2

    Poloxamer 407
    .....

    "To mimic the increased TGRL levels observed in many patients with metabolic disorders, we used the poloxamer 407 (P-407)-induced model of dyslipidemia (Johnston, 2004). This chemically induced model of hyperlipidemia involves the intraperitoneal (i.p.) administration of the non-ionic surfactant P-407 to wildtype C57BL/6 (B6) mice on chow diet and allows for a dosecontrolled dyslipidemia."

    Link to study
     
  4. haidut

    haidut Member

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    So, the proper title of the study should be "Hyperlipidemia promotes inflammation". Aside from the fact that saturated fat is not a direct precursor to inflammatory mediators (unlike the PUFA arachidonic acid), Peat has consistently been recommending oxidizing sugar instead of fat, noting that even saturated fat oxidation can in the long run produce undesirable effects on metabolism. Oxidizing fat, saturated or not, is a sign of stress and leads to all the stress-induced adaptations.
    PUFA Promote Stress Response; Saturated Fats Suppress Stress Response – Functional Performance Systems (FPS)
    "...“I’ve known people who were eating 2-3 pounds of meat a day and who were getting sicker and sicker as their free fatty acids and free amino acids increased. That started me reading more about the free state of fatty acids in the blood. Just about everything that goes wrong, involves free fatty acids increase. If they’re totally saturated fatty acids, such as from coconut oil and butter, those are less harmful, but they still tend to shift the mitochondrial cellular metabolism away from using glucose and fructose, and turning on various stress-related things (by lowering the carbon dioxide production, I think, is the main mechanism).”
     
  5. Giraffe

    Giraffe Member

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    Thanks for suggesting an appropriate title. I changed it.
     
  6. PakPik

    PakPik Member

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    One may argue that since PUFAs can have very potent immunosuppressive actions, if saturated fats inhibit those PUFA actions they may act "pro-inflammatory" that way. That said, there's recent evidence that satturated fatty acids may directly stimulate proinflammatory signaling, but I don't know how to judge the validity of that study Saturated fatty acids activate TLR-mediated proinflammatory signaling pathways. - PubMed - NCBI

    "Toll-like receptor 4 (TLR4) and TLR2 were shown to be activated by saturated fatty acids (SFAs) but inhibited by docosahexaenoic acid (DHA). However, one report suggested that SFA-induced TLR activation in cell culture systems is due to contaminants in BSA used for solubilizing fatty acids. This report raised doubt about proinflammatory effects of SFAs. Our studies herein demonstrate that sodium palmitate (C16:0) or laurate (C12:0) without BSA solubilization induced phosphorylation of inhibitor of nuclear factor-κB α, c-Jun N-terminal kinase (JNK), p44/42 mitogen-activated-kinase (ERK), and nuclear factor-κB subunit p65, and TLR target gene expression in THP1 monocytes or RAW264.7 macrophages, respectively, when cultured in low FBS (0.25%) medium. C12:0 induced NFκB activation through TLR2 dimerized with TLR1 or TLR6, and through TLR4. Because BSA was not used in these experiments, contaminants in BSA have no relevance. Unlike in suspension cells (THP-1), BSA-solubilized C16:0 instead of sodium C16:0 is required to induce TLR target gene expression in adherent cells (RAW264.7). C16:0-BSA transactivated TLR2 dimerized with TLR1 or TLR6 and through TLR4 as seen with C12:0. These results and additional studies with the LPS sequester polymixin B and in MyD88(-/-) macrophages indicated that SFA-induced activation of TLR2 or TLR4 is a fatty acid-specific effect, but not due to contaminants in BSA or fatty acid preparations"​
     
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