New Fluge & Mellas new metabolic profiling study

Strike me lucky

Well-Known Member
@Cort Reduced levels of BCAAs have been found in the Naviaux and Fluge & Mella studies too.

After reading the Naviaux paper, i took a punt on trying BCAAs. Difficult to be objective but I would say in association with Creatine, they have helped.
Hmb is a metabolite of one of the bcaa's that is said to be responsible for anabolic/anticatabolic effects of bcaa's. I have been using hmb and it does seem to help exercise recovery ie less post exercise stiffness. And some nutrient partitioning effects ie using calories more efficiently and not storing it all as fat??
 

Remy

Administrator
Hmb is a metabolite of one of the bcaa's that is said to be responsible for anabolic/anticatabolic effects of bcaa's. I have been using hmb and it does seem to help exercise recovery ie less post exercise stiffness. And some nutrient partitioning effects ie using calories more efficiently and not storing it all as fat??
I picked up HMB for some reason but then put it back down again for some reason that I cannot for the life of me remember...is it an arginine derivative? Hmmm.

Have you used the BCAA's too? Do you find that HMB is better?
 

Remy

Administrator
Also, this on lactate:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4777529/pdf/pone.0150303.pdf

"Earlier work suggests that blood lactate is elevated among obese, insulin-resistant subjects, and that blood lactate may be an independent risk factor for the development of type 2 diabetes [8–11].

Elevated lactate may promote hepatic gluconeogenesis and interfere with glucose uptake in the muscle by serving as a substitute for glucose utilization [12].

Lactate infusion also decreases glucose oxidation [13]. In 2010, a large sample retrospective study by Crawford and colleagues showed that plasma lactate was strongly associated with type 2 diabetes [14]. In 2013, a prospective study by Juraschek and colleagues reported that blood lactate predicted incident diabetes independent of many other risk factors and was strongly related to markers of insulin resistance [15]."

A compound called oxalate inhibits lactate dehydrogenase and decreases lactate levels. It has been identified as a target for treating diabetes and also epilepsy, both conditions which appear to have a metabolic basis at least somewhat related to MECFS.
 

Remy

Administrator
There is an "introduction" to pyruvate dehydrogenase metabolism here, but I warn you, it is an introduction in name only.

It is worth reading though because it's laid out about as clearly as anything I've seen.

The bulk of ATP used by many cells, to maintain homeostasis, is produced by the re-oxidation of the reduced electron carriers, NADH and FADH2, within the mitochondrial oxidative phosphorylation pathway. A large percentage of these two reduced electron carriers are generated by the oxidation of pyruvate in the TCA cycle. The fate of pyruvate depends on the cell energy charge. In liver, intestine, and kidney when the energy charge is high, pyruvate is directed toward gluconeogenesis. However, when the energy charge is low, pyruvate is preferentially oxidized to CO2 and H2O in the TCA cycle, with generation of 15 equivalents of ATP per pyruvate.
I'd quite like to know how one determines the cell energy charge?
 

Strike me lucky

Well-Known Member
I picked up HMB for some reason but then put it back down again for some reason that I cannot for the life of me remember...is it an arginine derivative? Hmmm.

Have you used the BCAA's too? Do you find that HMB is better?
Its a down stream metabolite of leucine. Generally make about 300mg a day but supplementing with it they recommend 1000mg 3 times a day. Prevents muscle damage and breakdown. One of its mechanisms is using cholesterol to repair damaged cells etc.

I do find after exercise im not as stiff and sore. Read it has a nutrient repartitioning effect which might br happening as my weight has increased slightly but waist and body fat stayed the same or decreased some.

Ive tried it a few times and theres something to it. When it came on the markey 20yrs ago it was quite expensive so got bad reviews as i think expectations were too high compared to the cost but now its much cheaper more people are trying it and more positive reviews .

The nutrient partitioning effects is probably a good thing for many of us if theres issues with insulin sensitivity and mito disorders. I guess its making nutrients more available instead of pushing it into fat storage .

I think many cfsers although not losing weight many seem to lose muscle and get fatter, body fat percentage goes up, in many for others they lose too much weight but either way i think cfsme contributes to catabolic muscle wasting in cfsme. Many have dodgy hormones which could also have catabolic effects too.
 
For PDK1 gene expression, there were significant associations with ME/CFS disease severity (higher PDK1 mRNA level in moderate/severe versus mild/mild-moderate groups), with ME/CFS disease duration (higher PDK1 mRNA level with increasing duration), and with physical activity level assessed as the mean steps per 24 hours (higher PDK1 mRNA level with lower activity) (Figure 3, N–P).
Others have highlighted that this indicates that PDK1 is a potential blood diagnostic marker. On the face of it either the activity of PDK1 enzyme could be used as the basis for a diagnostic test or the PDK1 mRNA level could be used. Does anyone know the costs of either of these approaches i.e. measuring the activity of the enzyme or mRNA level? Are there currently normal values for the activity of the enzyme, and/or mRNA level, i.e. to compare to the levels in people with ME/CFS?

On the face of it tests based on the activity of the enzyme, and/or mRNA level, could be scaled up to deal with the number of people with ME/CFS since these appear to be relatively rapid tests which can be automated.
 

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