Sunday Science by GoUnPro 2026_11_01 Lipid Lengthening and Aging

Welcome to Sunday Science, where we dive into a few recent scientific articles and their translation into our modern lives. Here is your host, Brent W. Laartz, MD. All right, everyone. All right, everyone. Welcome to Go Un Pro Sunday Science. Here we are Sunday, November 1st, Halloween yesterday. Here in Florida, it was raining. And what we're talking about today is a neat study that came out here in October, just last month. And it is about... lipid lengthening and aging. So we've heard about telomere lengthening. We've heard about protein glycation, DNA methylation, et cetera, as markers of aging. Another example now that we potentially have based on this study and some other referential studies is lipid chain elongation. So The age of C.

elegans, Drosophila, mice, and humans, all four of these in this study were looked at and It is seen with these that there is a gene, PLB1 expression, and a couple of other genes, ELO1, ELO2, ELO5, that seem to be downstream of each other. And according to this study, lipid length in membranes is associated with aging. So the longer the lipids, the law more age and etc and okay so we'll go through this a little bit all right so let's get to a couple of the studies first and I’ll just show you just a let's go through a schematic here of how this might work okay so I’m going to share We're going to share the screen. We’ll put me in the background here and we'll go to share.

Okay, so here we are with this Manifesting 111. Love it. Sunday Science Lipid Length by Go On Pro, the podcast. All right, so the schematic here is, if you look at this lipid metabolism, there is an enzyme called ELOVL. That is the elongation of lipids. Let me just pull it up here. And so this study is in the show notes. It is in Nature Aging. It is by Weisha Li et al. And it was October 6th, 2026 publishing date. Okay, again, in Nature Aging. All right, so these. ELOVL enzymes, which stands for elongation of very long chain fatty acids. So you can have fatty acids that are by themselves, very long chain fatty acids, or you can incorporate this into triglycerides. And the same thing would be in...

So you can see in the upper left there, fatty acids are either short chain of two to five carbon. They're long chain between 13 and 21 and very long chain of 22 plus. So if you take those fatty acids and you go over to the right, and this is during anabolism. the ELOVL enzymes will lengthen by two carbon acyl, A-C-Y-L groups, and it takes a melanyl coA enzyme to do that. And melanyl coA is the... is the cofactor and it creates another two carbons. So you take the 16 and 18 carbon fatty acids and it will create very long chain fatty acids. And this leads then to, in the bottom right, cellular aging, membrane distortion and rigidification, mitochondrial dysfunction, senescence-associated secretory phenotypes, and endoplasmic reticulum. stress, okay?

But the opposite occurs with beta-oxidation on the left, okay? If you are looking at this on a video, beta-oxidation takes those fatty acids, 16, 18, 16, and potentially the 22 and greater very long-chain fatty acids, and catabolizes it and removes a two carbon length and a set of CoA and basically then cleaves those and removes them in the peroxisome in the mitochondria and actually creates a better function here. Okay, so that is the schematic here. Here on the screen here is the. citation here. So what they did was they showed that this was associated with age, with these very long chain fatty acids, and it's also associated with heart disease progression in the membranes of cardiac cells. Then they took these mice and also in vitro and tried to manipulate it by using some interventions.

And it does decrease the lipid length if you treat with rapamycin in vitro, though if you give it in vivo treatment of rapamycin to mice, that it does only decrease the lipid length in certain fatty acids and with dietary restriction actually was the strongest and actually did globally decrease dietary calorie restriction decreased lipid length globally in all of the fatty acids found then they looked at this and were able to find four genes, PLB1, ELO1, ELO2, and ELO5, that seemed to be downstream of each other because knockouts of these genes increased the frailty index and also knockouts extended the lifespan of these organisms. And they seem to be downstream of each other because all four of them, if you knocked out one, knocking out another one did not decrease the lifespan any further. And it also didn't decrease the lipid length any further either. It appears to be through mitochondrial Endo lysosomes and plasma membrane effects. Based on also some other portions of this study. It's a good read in and of itself. The because of the issues here with busyness of these graphics that it had in here.

See, we're removing the share. Let's get off of this share. Why isn't it taking off the share here anyway? So we're trying to get rid of this share here.

There we go. I don't know why I lost that. All right, so now we're back. All right, so here we are again with this study, and obviously this is some of the first studies of their kind, and so there's a lot more work to be done to show whether or not this... gene expression, PLB1, ELO1, ELT, ELO2, ELO5, and whether this ELOVL lengthening associated with age is true. It will be interesting to see that we already know that calorie restriction is associated with increased lifespan. It's associated also with decreased lipid length as well. and decreased PLB1 expression. And also then that PLB1 expression, if it is knocked out of these mice, then it can increase lifespan and seems to be downstream of each other. So interesting findings. It could be another potential.

marker of biomarker of aging that they could use in addition to telomere lengthening, protein glycation, DNA methylation, et cetera, that are the hallmarks of aging and the biomarkers of aging. So this lipid chain elongation. Again, thank you for joining me for Sunday Science. And again, in the show notes will be. The citation here of Weisha Li et al .Longer lipids mark aging and constrain lifespan from nature aging. Volume 6, 2026. 2074 to 2091 is the pages. Okay, so again, thanks for joining me. Sunday Science, we're going to also probably in one or two weeks have a really good review of microbiome and aging and a good study there. So again, look for us again on the Sunday Science. Good to see you guys. Thanks for joining me on Sunday Science. Thanks.

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Li, W., Schomakers, B.V., Trętowicz, M.M. et al. Longer lipids mark aging and constrain lifespan. Nat Aging 6, 2074–2091 (2026). https://doi.org/10.1038/s43587-026-01223-x