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. 2022 Aug 11;13:927763. doi: 10.3389/fendo.2022.927763

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Copyright © 2022 Tang, Ma, Gao, Zeng, Feng, Guo, Hu, Yang, Chen, Zhang, Yuan and Guo

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic representation of the proposed mechanism by which ANGPTL8 induces ectopic lipid deposition by promoting adipogenic differentiation of mesenchymal stem cells. The elevated fatty acid levels upon long-term exposure to an HFD upregulate liver ANGPTL8. ANGPTL8, in turn, secreted by the liver into the blood, acts on MSC cells in various organs. Secreted ANGPTL8 upregulates the expression of PPARγ and c/EBPα by inhibiting the Wnt/β-catenin signaling pathway and promotes the adipogenic differentiation of MSCs, resulting in lipid deposition in multiple organs and causing obesity in male mice. Estrogen can inhibit the expression of ANGPTL8 to counteract the effect of ANPTL8 KO on obesity in female mice.