Oxalate Dumping - a Probiotic Solution?

[Violeta]

That's the same study, @Gondwanaland, it says aldehyde glyoxalate levels increased before glucose levels increased. There is no glyoxalate cycle in humans.

 

[Gondwanaland]

That's the same study, @Gondwanaland, it says aldehyde glyoxalate levels increased before glucose levels increased. There is no glyoxalate cycle in humans.

Now I am confused

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4265698/#B18
Glyoxylate in its metabolic network may serve as an early marker in diabetes diagnosis with predictive qualities for associated complications and as potential to guide the development of new antidiabetic therapies.

I think that is in humans
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3139422/figure/F4/

Plus:

http://www.ncbi.nlm.nih.gov/pubmed/2208646/
The parenteral nutrient xylitol, the hyperosmolar agent glycerol, the polysorbate emulsifiers (e.g., in vitamin E preparations), the anesthetic methoxyflurane, and possibly the experimental hypoglycemic agent dichloroacetate all produce a toxicity syndrome very similar to that of ethylene glycol poisoning.

so that is how polyols end (I wonder if all of them?)

 

[Violeta]

Now I am confused

I think that is in humans
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3139422/figure/F4/

Plus:

so that is how polyols end (I wonder if all of them?)

So am I, but I'm sorry for any confusion I caused.

I just found this:

In the liver of herbivorous animals and man, serineyruvate/alanine:glyoxylate aminotransferase (SPT/AGT) locates in peroxisomes, and plays an important role of removing glyoxylate by transamination to Gly. Primary hyperoxaluria type 1 (PH1), a congenital metabolic disease characterized by increased oxalate production and precipitation of calcium oxalate crystals in many tissues, is caused by a defect in SPT/AGT."

So maybe this is what I was supposed to understand from the beginning. I don't know.

Strange no elevated oxalates????

PS: I did not put that emoticon in there I don't have any idea how it got there.

 

[Gondwanaland]

PS: I did not put that emoticon in there I don't have any idea how it got there.

you need to put a space between : and p

I am schocked reading the paper about polyols
http://www.clinchem.org/content/36/10/1717.long

 

[Violeta]

you need to put a space between : and p

I am schocked reading the paper about polyols
http://www.clinchem.org/content/36/10/1717.long

I don't know what polyols are, I have to do some reading, as soon as I give my dog her bath and comb her out.

Please look at this and see if you can dumb it down for me.

"Oxalate synthesis in human hepatocytes is not well defined despite the clinical significance of its overproduction in diseases such as the primary hyperoxalurias. To further define these steps, the metabolism to oxalate of the oxalate precursors glycolate and glyoxylate and the possible pathways involved were examined in HepG2 cells. These cells were found to contain oxalate, glyoxylate, and glycolate as intracellular metabolites and to excrete oxalate and glycolate into the medium. Glycolate was taken up more effectively by cells than glyoxylate, but glyoxylate was more efficiently converted to oxalate. Oxalate was formed from exogenous glycolate only when cells were exposed to high concentrations. Peroxisomes in HepG2 cells, in contrast to those in human hepatocytes, were not involved in glycolate metabolism. Incubations with purified lactate dehydrogenase suggested that this enzyme was responsible for the metabolism of glycolate to oxalate in HepG2 cells. The formation of 14C-labeled glycine from 14C-labeled glycolate was observed only when cell membranes were permeabilized with Triton X-100. These results imply that peroxisome permeability to glycolate is restricted in these cells. Mitochondria, which produce glyoxylate from hydroxyproline metabolism, contained both alanine:glyoxylate aminotransferase (AGT)2 and glyoxylate reductase activities, which can convert glyoxylate to glycine and glycolate, respectively. Expression of AGT2 mRNA in HepG2 cells was confirmed by RT-PCR. These results indicate that HepG2 cells will be useful in clarifying the nonperoxisomal metabolism associated with oxalate synthesis in human hepatocytes."

 

[alicec]

5 ml is a really tiny amount

Well it's far more than you'll ever get in a bath or foot bath. This is a saturated solution, so in round figures, 700 mg/ml (roughly 10% magnesium, 40% sulfate). With a generous 500 g Epsom salt into an average bathtub, you'd end up with around 2.5 mg/ml.

The entire 5 ml is applied to and absorbed by the skin. In a bath, an unknown amount wafts by the body and an even smaller amount is absorbed.

 

[alicec]

Just a practical question...Do you make it up in large batches? Very hot water? Least itchy places to apply? I have been buying Ancient Minerals Magnesium Lotion.

I make up a batch of 250 ml (just because I happen to have a 250 ml bottle with a flip cap). 70g/100 ml is a roughly saturated solution. Often I use 65g/100 ml so there is not too much crystallisation over time.

Use pharmaceutical grade Epsom salts (the cruder stuff might be ok dissolved in a large bathful of water but I don't fancy the concentrated impurities on my skin). Just weigh out the salts into a small measuring jug and add boiling water to the appropriate mark.

Stir a few times until the salts dissolve. When cool, pour into a bottle. I once used a bottle with eyedropper and could work out what volume I was using. I got tired of crystals clogging the dropper and changed to a flip top. I just roughly gauge the volume by looking at it in my hand.

The magnesium lotion is magnesium chloride. It's a good source of magnesium but of course no sulfate.

Actually I use a mixture of both. Approx 5 ml of the sulfate solution (which I apply to trunk and inner arms) and 5 ml of magnesium oil to muscles and sore spots (the entire body is now pretty much covered in some form of magnesium!), then lots of body lotion since both of the solutions are drying/irritating.

I did try just using the sulfate solution (certainly a cheaper option) but it didn't give as much relief to muscle ache so I came up with the mixture.

 

[alicec]

What is aldehyde glyoxylate

It's just a description of the class of compound that glyoxylate belongs to. Glyoxylate is an aldehyde.

 

[alicec]

So maybe this is what I was supposed to understand from the beginning

Well that is what we have been discussing on and off since the beginning of this thread (and previously on the CB thread which this spun off from.

 

[Violeta]

It's just a description of the class of compound that glyoxylate belongs to. Glyoxylate is an aldehyde.

Thanks, @alicec .

"Oxalate synthesis in human hepatocytes is not well defined despite the clinical significance of its overproduction in diseases such as the primary hyperoxalurias. To further define these steps, the metabolism to oxalate of the oxalate precursors glycolate and glyoxylate and the possible pathways involved were examined in HepG2 cells. These cells were found to contain oxalate, glyoxylate, and glycolate as intracellular metabolites and to excrete oxalate and glycolate into the medium. Glycolate was taken up more effectively by cells than glyoxylate, but glyoxylate was more efficiently converted to oxalate. Oxalate was formed from exogenous glycolate only when cells were exposed to high concentrations. Peroxisomes in HepG2 cells, in contrast to those in human hepatocytes, were not involved in glycolate metabolism. Incubations with purified lactate dehydrogenase suggested that this enzyme was responsible for the metabolism of glycolate to oxalate in HepG2 cells. The formation of 14C-labeled glycine from 14C-labeled glycolate was observed only when cell membranes were permeabilized with Triton X-100. These results imply that peroxisome permeability to glycolate is restricted in these cells. Mitochondria, which produce glyoxylate from hydroxyproline metabolism, contained both alanine:glyoxylate aminotransferase (AGT)2 and glyoxylate reductase activities, which can convert glyoxylate to glycine and glycolate, respectively. Expression of AGT2 mRNA in HepG2 cells was confirmed by RT-PCR. These results indicate that HepG2 cells will be useful in clarifying the nonperoxisomal metabolism associated with oxalate synthesis in human hepatocytes."

Thanks, @alicec , and are you able to dumb this down for me?

 

[Gondwanaland]

I don't know what polyols are,

Sugar substitutes Sorbitol Xylitol Erithritol

I don't think the text you are interested in is really relevant... It is a description of the in vitro experiment with glycine metabolites

 

[alicec]

are you able to dumb this down for me?

HepG2 is a cell line derived from a human liver carcinoma. Essentially they are examining various aspects of oxalate-related metabolism in the cell line to determine if it coincides with what is known about oxalate metabolism in whole living humans.

They decide that is does (although peroxisomes seem to behave a bit differently) and so think the cell line will be useful for studies trying to understand previously poorly understood aspects of oxalates.

 

[alicec]

Now I am confused

The glyoxylate cycle is different from the pathway you link.

It is a truncated form of the Kreb's cycle. We have mentioned it previously but it is a bit of a side issue. The critical enzymes for it do indeed exist in humans and it seems it might operate under some conditions but it is not well understood.

The pathway you link and which we have discussed many times remains central to the whole oxalate problem.

 

[alicec]

would a diet with high fat content (but not low carb) help to bind and excrete oxalates

It might do the opposite if there were digestive problems. Undigested fat would form insoluble soaps with calcium ions which would then be unavailable to bind and remove oxalates. This is a notable problem in autistic children.

 

[Gondwanaland]

it might operate under some conditions but it is not well understood.

The connection with insulin resistance/pre-diabetes made sense to me

 

[alicec]

The connection with insulin resistance/pre-diabetes made sense to me

The connection is occurring though the usual pathways of which AGT is the lynchpin - the same pathways you have linked above and previously and which we have discussed often on this thread. This is NOT the glyoxylate cycle. The latter is an entirely separate metabolic pathway of great relevance in plants which maybe operates in humans under some conditions but is not well understood.

The terms are confusing I know but really the glyoxylate cycle is a diversion. Just focus on the pathways centred on AGT and you will be able to follow how oxalate spreads its terrible metabolic effects so widely.

 

[Gondwanaland]

I was thinking more in the line like B6 being diverted towards glucose metabolism and then there is not enough B6 to avoid endogenous formation of oxalates. Like I recently experienced anaphylaxis and hive from taking Biotin - all of a sudden I didn't have enough B6 for dietary amines because biotin antagonizes it in the glucose metabolism.

 

[alicec]

I was thinking more in the line like B6 being diverted towards glucose metabolism and then there is not enough B6 to avoid endogenous formation of oxalates. Like I recently experienced anaphylaxis and hive from taking Biotin - all of a sudden I didn't have enough B6 for dietary amines because biotin antagonizes it in the glucose metabolism.

Yes that is all fine.

Maybe I got confused because you linked to my comment on the glyoxylate cycle.

Everything all comes back to the B6 dependant AGT.

 

[Gondwanaland]

Does anyone here uses lymphocyte count to track B6 deficiency? I just realized that it is an excellent marker for that, I guess even better than homocysteine.

 

[Gondwanaland]

Maybe allithiamine competes somehow with something that precipitates dumping?

It probably contains plenty of sulfate, making the oxalates go away via urine painlessly.

I have noticed consistent oxalate dumping, several times a week, at a tolerable level. I haven't changed anything else that might precipitate oxalate dumping so this could well be due to the probiotic.

Do you think it is possible that this probiotic induces endogenous oxalate formation in erythrocytes rather than anything else?

http://www.nature.com/nrneph/journal/v4/n7/pdf/ncpneph0845.pdf
Oxalate is obtained from diet, degradation of ascorbate, and synthesis by the liver and erythrocytes