A highly saturated fat-rich diet is more obesogenic than diets with lower saturated fat content
and is looking at this graph:
Again, this post is pure speculation. I don't even know if the lab had a janitor.
The red oval highlights a serious "That's odd" moment. With this sort of finding you can
a) Say "That's odd" and think about investigating it based on what probably happened.
b) Report it, accept that you have no idea what it is all about and say so.
c) Pretend it didn't happen, but leave the anomaly in the graph without mentioning it in the results or discussion.
d) Falsify the data.
To their credit the group took option c), as far as I can glean after making myself read the results and skim-read the discussion section. The didn't take option d), to their slight credit.
Why do I find this so interesting?
Because rats, subjected to a 40% reduction (down to 165kJ/d) in available calories from their preferred calorie intake (270kJ/d) quite suddenly, after about 10 days of clearing the food hopper, started to leave some of the full (but small) amount of offered food.
In real terms this means that, suddenly, they weren't hungry. During a 40% calorie restriction.
Just think about that.
Nothing at all is reported to have changed at the time point of the sudden drop in hunger.
Oooooh, now that's a challenge if ever I saw one. The change was transient and the rats were almost back to clearing their hopper at the time they were executed ("euthanised" under CO2 anaesthesia).
Aside: If you have an anaesthetic machine with a CO2 regulator and a cylinder of CO2 you can easily dial a 50:50 mixture of CO2:O2 and try inhaling it. I would suggest that is no fun. No fun at all. I guess the study's ethics committee have never tried this. Maybe they don't have an anaesthetic machine with a CO2 regulator to try it with. The way I used to have. End aside.
Anyhoo. Here's a Powerpoint of lines popping up on diagrams.
TLDW?
The janitor turned up the heating. Day 109.
Peter
PS this wouldn't work in humans, not even transiently. We're too big, we live very close to our thermoneutral point compared to rats.
Links to papers briefly used in the presentation.
Mouse EE graph from https://pubmed.ncbi.nlm.nih.gov/26042200/
Mouse to rat EE conversion from
2 comments:
Apologies for the totally off-topic question. Is this new information, and is there anything to it, about distinct subpopulations of mitochondria?
https://www.nature.com/articles/s41586-024-08146-w
https://www.youtube.com/watch?v=QKOdGCy34Xw
Hi cave,
I'd not come across that but it fits perfectly well with the clash between ox-phos and anabolic functions of the mitochondria which Nick Lane discussed in Transformer. We also know that ATP for growth can (and is, under tissue repair for example) be derived from glycolysis in addition to ox-phos. I can conceive that sub populations exist where some mitochondria do ox-phos and some do anabolism in the same cell.
As another thought: If you assume that cancer is response to an unsuppressable growth signal then I can see a drive to subsume all mitochondria to the anabolic state, decrease cristae and use glycolysis or glutamate catabolism for substrate level phosphorylation of ADP. That might end up giving you the grossly abnormal mitochondria seen in EMs of aggressive cancer cells. Just a thought...
Peter
BTW on the Youtube page was a link to China licensing two experimental thorium reactors, so that was another rabbit hole. I seem to have been corrupted by Arnaud Bertrand on X to modify my MSM influenced discomfort about China. Though they clearly did as badly as the rest of us over Covid!
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