New Atmosphere, New Vision: Gibson and Whittemore Kick Off Invest in ME Conference 2016
Mark Berry reports on Dr. Gibson's introduction and Dr. Whittemore's keynote speech, at the 11th Invest in ME International ME Conference in London.
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NAFLD & impaired lipid metabolism

Discussion in 'General ME/CFS News' started by aquariusgirl, Jul 9, 2017.

  1. aquariusgirl

    aquariusgirl Senior Member

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    • This is not ME/CFS research per se.. but I thought it was on point...considering Bob Naviaux's work on lipids. Also, some of use have reported having NAFLD.



    IUBMB . 2017 Apr;69(4):263-270. doi: 10.1002/iub.1613. Epub 2017 Mar 8.
    The role of insufficient copper in lipid synthesis and fatty-liver disease.
    Morrell A1, Tallino S1, Yu L2, Burkhead JL1.
    Author information

    Abstract
    The essential transition metal copper is important in lipid metabolism, redox balance, iron mobilization, and many other critical processes in eukaryotic organisms. Genetic diseases where copper homeostasis is disrupted, including Menkes disease and Wilson disease, indicate the importance of copper balance to human health. The severe consequences of insufficient copper supply are illustrated by Menkes disease, caused by mutation in the X-linked ATP7A gene encoding a protein that transports copper from intestinal epithelia into the bloodstream and across the blood-brain barrier. Inadequate copper supply to the body due to poor diet quality or malabsorption can disrupt several molecular level pathways and processes. Though much of the copper distribution machinery has been described and consequences of disrupted copper handling have been characterized in human disease as well as animal models, physiological consequences of sub-optimal copper due to poor nutrition or malabsorption have not been extensively studied. Recent work indicates that insufficient copper may be important in a number of common diseases including obesity, ischemic heart disease, and metabolic syndrome. Specifically, marginal copper deficiency (CuD) has been reported as a potential etiologic factor in diseases characterized by disrupted lipid metabolism such as non-alcoholic fatty-liver disease (NAFLD). In this review, we discuss the available data suggesting that a significant portion of the North American population may consume insufficient copper, the potential mechanisms by which CuD may promote lipid biosynthesis, and the interaction between CuD and dietary fructose in the etiology of NAFLD. © 2016 IUBMB Life, 69(4):263-270, 2017.

    © 2017 International Union of Biochemistry and Molecular Biology.
     
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  2. drob31

    drob31 Senior Member

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    I'm genetically predisposed to NAFLD. With impaired lipid metabolism, I'm assuming avoid fats? Paleo, low card would be a terrible idea?
     
  3. aquariusgirl

    aquariusgirl Senior Member

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    • PMID: 27587995

    • Send to



      Front Mol Neurosci. 2016 Aug 18;9:68. doi: 10.3389/fnmol.2016.00068. eCollection 2016.
      Metal-Dependent Regulation of ATP7A and ATP7B in Fibroblast Cultures.
      Lenartowicz M1, Moos T2, Ogórek M1, Jensen TG3, Møller LB4.
      Author information

      Abstract
      Deficiency of one of the copper transporters ATP7A and ATP7B leads to the rare X-linked disorder Menkes Disease (MD) or the rare autosomal disorder Wilson disease (WD), respectively. In order to investigate whether the ATP7A and the ATP7B genes may be transcriptionally regulated, we measured the expression level of the two genes at various concentrations of iron, copper, and insulin. Treating fibroblasts from controls or from individuals with MD or WD for 3 and 10 days with iron chelators revealed that iron deficiency led to increased transcript levels of both ATP7A and ATP7B. Copper deficiency obtained by treatment with the copper chelator led to a downregulation of ATP7A in the control fibroblasts, but surprisingly not in the WD fibroblasts. In contrast, the addition of copper led to an increased expression of ATP7A, but a decreased expression of ATP7B. Thus, whereas similar regulation patterns for the two genes were observed in response to iron deficiency, different responses were observed after changes in the access to copper. Mosaic fibroblast cultures from female carriers of MD treated with copper or copper chelator for 6-8 weeks led to clonal selection. Cells that express the normal ATP7A allele had a selective growth advantage at high copper concentrations, whereas more surprisingly, cells that express the mutant ATP7A allele had a selective growth advantage at low copper concentrations. Thus, although the transcription of ATP7A is regulated by copper, clonal growth selection in mosaic cell cultures is affected by the level of copper. Female carriers of MD are rarely affected probably due to a skewed inactivation of the X-chromosome bearing the ATP7A mutation.

      KEYWORDS:
      copper; iron–copper interaction; menkes disease; regulation; wilson disease

      PMID:

      27587995

      PMCID:

      PMC4988979

      DOI:

      10.3389/fnmol.2016.00068
      Free PMC Article
     
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  4. Crux

    Crux Senior Member

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    USA
    Without sufficient copper, iron accumulates in the liver. This can cause fatty liver, cirrhosis, and even cancer.

    Thanks aquariusgirl.
     

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