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oxolates & glucose

Discussion in 'General Treatment' started by aquariusgirl, May 2, 2017.

  1. aquariusgirl

    aquariusgirl Senior Member

    For those of you interested in the role of oxolates in our illness, I wanted to draw your attention to this paper & to point out the authors' assertion that glucose is converted to oxolate in the presence of copper 2 and iron 3.

    Also, if you check out Fig 1 in the paper, you will notice that copper 2 is essential for 2 pathways that wind up generating oxolate.

    William Shaw at Great Plains has talked about ascorbate converting to oxolate in the presence of free copper but I haven't heard anything about this other pathway & I wonder if this ties in with the findings of Fluge & Mella & the australians with respect to pyruvate dehydrogenase.

    I'm assuming that results in elevated glucose if a person keeps eating carbs. So my clumsy guesswork is ...elevated glucose in the presence of free copper & iron = lots & lots of oxolates.

    So I wonder if we need a low glucose diet, not a low oxolate diet, as well as therapies to lower ROS, to stop our cells turning into oxolate factories?

    Quotes from the paper:

    The biochemical pathways involved in oxalate production are poorly understood despite decades of research.However, it is clear that glyoxylate is the major precursor of oxalate [1].

    We hypothesize that glyoxal is one of the most important sources of endogenous oxalate synthesis in humans.

    In addition to the many exogenous sources of glyoxal, it is endogenously produced via autoxidation of carbohydrates and ascorbate, degradation of glycated proteins and lipid peroxidation [9].

    Glyoxal can be formed through various pathways as illustrated in Figure 1.

    It is created directly from glucose via retroaldol condensation, and it is formed indirectly from glucose via a glycoaldehyde intermediate that undergoes autoxidation. The autoxidation reaction is promoted by the presence of phosphate buffer and trace metal ions (Fe3+ and Cu2+) in solution.

    Manini et al. have demonstrated that glyoxal cannot only be formed from glucose but from many other carbohydrates as well, including galactose, mannose, fructose, ribose, arabinose, ribulose, glyceraldehyde, acetone, adenosine, mannitol, and glycerol [12].
  2. alicec

    alicec Senior Member

    The review is drawing our attention to glyoxal, to the fact that it can be formed from oxidation of carbohydrates (in particular glucose) and to its contribution to endogenous oxalate production.

    @aquariusgirl is wondering if recent studies showing defects in energy metabolism in ME/CFS might mean we are particularly susceptible to this potential source of (yet more) problems and further, because of statements about copper and iron ions in the review, do these metals play a special role.

    Regarding energy metabolism, I think it's hard to say if there are special implications for us. Chris Armstrong's studies did suggest that blood glucose was elevated in ME/CFS patients (see this thread for discussion). Fluge and Mella didn't look at this directly but their studies suggest that glucose is converted to pyruvate ok, the problem arises after that. Accumulating pyruvate is converted to lactate which might rise abnormally, but there's no particular reason to expect glucose to be elevated.

    It might depend more on the individual. Anyone with poor blood sugar control for whatever reason should certainly be alert to this possibility.

    The statements about copper and iron shouldn't be interpreted literally. The authors are referring to in vitro studies where a glucose solution was held at 37 deg C for up to 3 weeks and formation of glyoxal and other substances was measured. Incubation conditions were varied to gain insight into mechanism of conversion.

    For the reaction to proceed, ie for glyoxal to be formed from glucose, a reasonable concentration of phosphate buffer was required while the addition of a chelating agent prevented formation.

    This result means simply that an oxidation reaction is involved in the conversion. To understand the reasoning behind this conclusion you need to understand that the chelating agent removes metal ions, these in turn are oxidising agents and the source of the metal ions is the phosphate buffer, since metals are common trace contaminants. There's no special role for the metal ions here, just as non-specific oxidising agents.

    Redox conditions in the cell would determine whether such auto-oxidation reactions proceeded in vivo.

    I don't think the authors do a very good job of explaining what they mean here.

    So yes, we should be alert to this aspect of carbohydrate metabolism, especially if we know we have poor blood sugar control. This could be a significant contributor to glyoxalate accumulation and so to oxalate formation. We shouldn't forget though that how well or badly we deal with endogenous oxalate ultimately depends on our ability to siphon off glyoxylate into harmless glycine.

    Fig 3 in the review illustrates the pathways.
    Asklipia, Gondwanaland and Valentijn like this.
  3. aquariusgirl

    aquariusgirl Senior Member


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