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. 2021 Nov 30;53(11):1697–1705. doi: 10.1038/s12276-021-00712-w

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© The Author(s) 2021

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 — Circulating FAs are imported via FATPs, including CD36, FATP2, and FATP5. ACSL converts the FAs taken up by cells to acyl-CoA, which is further reesterified to produce glycerolipids, mainly in the ER. In addition, FAs can be synthesized via DNL using acetyl-CoA. These intracellular FAs can be consumed to generate VLDL by forming a complex with ApoB100 via MTP. Furthermore, FAs are cleaved to generate acetyl-CoA through FA oxidation in the mitochondria to produce ATP and ketone bodies. An imbalance between lipid disposal and storage promotes fatty liver disease.