Discussion in 'BioMedical ME/CFS Research' started by hixxy, Apr 16, 2018 at 12:34 AM.
A pdf of the accepted manuscript (not the final version) is here
Interesting- potential upstream modulation paths mentioned ( including liver which has always been my hunch as part of the issue with my aunt and daughter).
There were a few very interesting threads involving AMPK' s potential role in the other place.
I have no idea what AMPK is or does. I googled and found this incredibly complicated diagram. My head exploded.
This was a little more helpful:
I keep saying there is an issue with glucose. Maybe I'm actually right
Fukuda selection criteria with no mention of PEM again. I appreciate Newton for plugging away in the UK with biomedical studies but, in my opinion, she needs to change the criteria she uses.
AMPK is also involved in " clock" processes, and could be significant in Naviaux's hypometabolic state hypothesis....
So much of this chimes with me.
From the other place - a few threads
AMPK in blood cell deformity
AMPK role in M3 signalling
AMPK in purinergic signalling
AMPK and Metformin
A few days ago @Skycloud started this thread about Metformin trials with Lupus
It's an article from Science magazine
There's also a thread from AndyPandy who talks about their experiences withMetformin as a type 2 diabetic. They may be very different from people without Type 2 diabetes.
ME and Metformin
There's always a race to say this.
Is there? I wasn't aware of that.
How the study was funded
"Acknowledgements The work was funded by ME Research UK and supported by the NIHR Newcastle Clinical Research Facility."
From the discussion
"The important findings from this study are that, firstly, pharmacological activation of AMPK can improve glucose uptake in skeletal muscle cell cultures from patients with ME/CFS and secondly, cellular ATP content is significantly reduced in ME/CFS muscle cell cultures.
The observation that AMPK was activated directly by metformin and 991 but not EPS (electrical pulse stimulation) in the ME/CFS cultures points to a signalling defect proximal to AMPK"
Like @Trish, I've been trying to understand AMPK signalling without causing instant brain fog. Found this video on YouTube, which has enlightened me slightly.
Out of many things AMPK does, it instructs cells to take in more glucose to make more ATP and to store less glucose as glycogen (in the liver) when the ratio of ATP drops.
You can see the point if the AMPK signalling is messed up, it could cause energy shortages. (my non bio-chemist take)
I'll shut up now & let the proper experts correct me and take over. @Simon M is a proper biochemist not a 5 minute one
I found some AMPK activators for a blog post 3 years ago
I’ve been thinking about my very fluctuating ME journey over the last 20 years. I’ve been around 10% and around 95% on the Bell Disability Scale and everything in between up and down at different times. This week I’ve been thinking about when I went from 10% to 30% in a couple of weeks (with the help of a nutritionist). It could be a number of things but I started this supplement (Fast & be clear) at that point
My understanding is Quercetin, alpha lipoic acid, grapes and green tea are AMPK activators. I wonder if this was part of the benefit of taking this supplement?
That's exactly why I think the argument that doctors should already have a test for everything important is extremely silly and ignorant. Because metabolism is extraordinarily complex, and even all the complicated stuff that's known is not all of it yet.
Cellular ATP content bring low is what Myhill, Booth et al found, together with low cellular magnesium bound ATP ( not active without Mg)
I hate my phone - the keypad numbers are too small!!!!
Separate names with a comma.