In mice, of course. What are the broader implications of this supposed to be?
Fasting in mice turns on SIRT3 which requires NAD+ and this newly discovered gene SLC25A51 is involved in transporting NAD+ to SIRT3. There's plenty of data that shows mice can live 30% longer when calorie-restricted due to sirtuins being activated..
Anyone who's ever listed to Dr. David Sinclair speak about longevity, he almost always talks about how NAD+ is possibly the most important chemical in the human body, since we'd be "dead in 30 seconds" without it.
Sirtuins are the longevity genes that are activated when organisms are under duress, which can be simulated by fasting. Your body doesn't know when you're going to eat again, so the sirtuins get activated.
I wouldn't be surprised if researchers and labs are looking for ways to activate SLC25A51 chemically to get the NAD+ flowing to SIRT3 without requiring fasting.
You can listen to David Sinclair and Rhonda Patrick get into the details of how all of this works: https://www.foundmyfitness.com/episodes/david-sinclair
It was disappointing to hear David Sinclair makes his own resveratrol… can’t get it
To what end ?
Fasting would be cheaper, easier and less time-consuming and would include all of the related, broad-spectrum effects that we also believe fasting may produce.
I guess if you're a pharma investor or existing, entrenched player it makes sense to go that direction.
As a consumer, however, I wonder why (pills that might convey a subset of the benefits of fasting) would be interesting in any way.
Because fasting is hard?
Sinclair, IMHO, is all protein and zero enzyme and that is his problem. Without enough zinc NMNAT will not function and will slow the SIRT cycle. And increasing SIRT activity by shoving NAD in the cell with out zinc will end up depleting zinc.
This study appears to show that fasting is related to inducing the gene Slc25a51 and improving those factors.
I guess this contributes to the body of science around the potential health benefits of fasting.
What would be scummy would be some pharmaceutical company discovering this, not releasing the information, and trying to develop (or worse, failing to develop) a drug on their own after internal research that was never released to the world.
We share 97% of our genes with mice. Our organ systems and metabolic pathways are extremely similar. Our homeostatic mechanisms are nearly identical.
Some mouse models don't carry over to us, to be sure. But the reality is that most do. Do we know for a fact that this paper applies to us? No. But it significantly updates our priors. And that's always noteworthy.
For example, fasting for several hours in mice and in humans are completely different things (a human would have to fast for days to get similar results).
Anyone have an idea?
https://www.understandinganimalresearch.org.uk/news/nine-out...
But to be fair, there's a huge failure rate for pharmaceutical drugs in general.
https://www.frontiersin.org/articles/10.3389/fendo.2021.6492... Literally no one talks about this in mice metabolic research. I would not be surprised if a huge majority of mouse researchers in diabetes are unaware.
Part of our message is basically what you just said. We have multiple examples of genes where mutations cause diabetes in humans but don't in mice.
The other one we have is the fact that human pancreatic beta cell lines in labs don't even 100% act like human pancreatic beta cells in humans.