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. 2023 Sep 1;55(9):1955–1973. doi: 10.1038/s12276-023-01071-4

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — The schematic depicts the mechanisms of bioactive lipids identified by the lipidomics approach in adipocyte metabolism. The ester bond formation of FAHFAs is catalyzed by ATGL, and 9-PAHSA enhances insulin-stimulated glucose transport by enhancing GLUT4 translocation via the GPR120/PI3K/AKT axis. 5- and 9-PAHSA promote insulin-mediated suppression of lipolysis in white adipocytes. 12,13-DiHOME induces FA transporter (CD36) translocation, elevating FA uptake and producing substrates for thermogenesis. 12-HETE stimulates the GsPCR/PI3K/mTORC2/AKT pathway, enhancing GLUT4 translocation and contributing to improved insulin sensitivity. Circulating FAs activate HNF4α, promoting the gene expression of CPT1, PPARα, OCTN2, and CrAT, and they mediate hepatic production of acylcarnitine, which then serves as fuel for β-oxidation.