From the subtitles :
'it looks like patients have problems transforming sugar to energy' (approx quote).
This is interesting to me as I (as others seem to) have problems with sugar. Too much goes right through me (I was prescribed lactulose many years ago for constipation and within minutes total runs - in contrast my wife was prescribed the same for constipation caused by codeine medication and after three days at full dose - nothing).
So if we can't transform sugar to energy what happens to it?
I have the runs, possibly pee some out but do we end up with high circulating blood sugar and run similar risks of problems such as peripheral neuropathies like diabetics? Do we gain weight?
You would think something would turn up on standard testing but maybe it's more subtle than a lack of insulin or insulin resistance?
There are alternative pathways, see here:
https://en.wikipedia.org/wiki/Pyruvic_acid#Biochemistry
https://en.wikipedia.org/wiki/Glycolysis
ATP can still be made via glycolysis, with pyruvate ending up as lactic acid or oxaloacetic acid or alanine. PDH just catalyses the conversion to acetyl-CoA. Intermediates can also be used, such as dihydroxyacetone phosphate which can lead to formation of glycerol-3-phosphate, and ultimately the formation of triglycerides.
Also note that increased SIRT4 shifts the focus of the cell away from catabolism and towards lipid anabolism. But also keep in mind that one of the key fatty acid synthesis pathways still requires Acetyl-CoA.
But in general, I think there is some evidence that suggests that ME could be an alternative metabolic syndrome. Some of the most interesting findings however have been in the opposite direction of the typical metabolic syndrome. But then a minority of patients either have or will develop (it doesn't seem to be at a rate higher than the normal population) type 2 diabetes, so who knows?