I've read through this paper once. It's pretty interesting mechanistically and shows how MUFAs (but not PUFAs or SFAs) extend lifespan in C. Elegans through germline - intestinal interaction in a H3K4me3 methyltransferase mechanism. It is from the Brunet lab at Stanford which has worked on MUFAs/lipids quite a bit.
Just thought I would drop it here and I might add some notes later.
Mono-unsaturated fatty acids link H3K4me3 modifiers to C. elegans lifespan
Abstract
Chromatin and metabolic states both influence lifespan, but how they interact in lifespan regulation is largely unknown. The COMPASS chromatin complex, which trimethylates lysine 4 on histone H3 (H3K4me3), regulates lifespan in Caenorhabditis elegans. However, the mechanism by which H3K4me3 modifiers affect longevity, and whether this mechanism involves metabolic changes, remain unclear. Here we show that a deficiency in H3K4me3 methyltransferase, which extends lifespan, promotes fat accumulation in worms with a specific enrichment of mono-unsaturated fatty acids (MUFAs). This fat metabolism switch in H3K4me3 methyltransferase-deficient worms is mediated at least in part by the downregulation of germline targets, including S6 kinase, and by the activation of an intestinal transcriptional network that upregulates delta-9 fatty acid desaturases. Notably, the accumulation of MUFAs is necessary for the lifespan extension of H3K4me3 methyltransferase-deficient worms, and dietary MUFAs are sufficient to extend lifespan. Given the conservation of lipid metabolism, dietary or endogenous MUFAs could extend lifespan and healthspan in other species, including mammals.
Mono-unsaturated fatty acids link H3K4me3 modifiers to C. elegans lifespan (PDF Download Available).
Available from: https://www.research...legans_lifespan [accessed Sep 23, 2017].
Edited by prophets, 24 September 2017 - 02:33 AM.
