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. Author manuscript; available in PMC: 2022 Apr 25.
Published in final edited form as: Ageing Res Rev. 2020 Oct 5;64:101188. doi: 10.1016/j.arr.2020.101188

Fig. 7.

Fig. 7.

Schematic representation of lipid metabolism. Underlined are metabolites and enzymes that were associated with lifespan extension. Red font color represents downregulation or depletion from food, while green font color represents overexpression or supplementation. Dashed line represents that multiple steps are involved. (A) In fatty acid metabolism, triglycerides can form saturated or unsaturated fatty acids. Higher levels of mono-unsaturated fatty acids (MUFAs) were associated with increased lifespan. Downregulation of diacylglycerol O-acetyltransferase (DGAT), elongases (ELO), and a desaturase converting MUFAs to PUFAs (FAT), as well as upregulation of the lipase LIPL was associated with lifespan extension. (B) In sphingolipid metabolism, palmitoyl-CoA is converted to ceramides, which can then form sphingomyelins. Downregulation of several enzymes, including serine palmitoyltransferase (SPT), sphingomyelinase (SMase), sphingomyelin synthase (Smsynthase), glucosylceramide synthase (PDMP), ceramidase, and ceramide synthase was associated with lifespan increase. (C) In diacylglycerol metabolism, diacylglycerol can be converted to 2-arachidonoyl-sn-glycerol (2-AG) or phosphatidic acid (PA). PA promotes TOR activity. Diacylglycerol lipase (DAGL-1) overexpression and diacylglycerol kinase (DGK) downregulation were associated with lifespan extension in worms.