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. 2021 Jun 7;12:3350. doi: 10.1038/s41467-021-23808-3

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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. 9 — CD36 expression in lymphatic endothelial cells (LECs) follows an increasing gradient from gut mucosa to submucosa to collecting mesentery vessels. CD36 deletion in LECs in adult mice (Cd36^ΔLEC) increases discontinuity of VE-cadherin junctions and associates with lymph leakage in the mesentery. Inflammation of visceral fat, age-associated obesity and glucose intolerance are observed in 20-week-old Cd36^ΔLEC mice. The mechanism likely involves reduced signaling of VEGF-C in LECs, which leads to disorganization of LEC junctions and impairs cell migration and tube formation. Image created using BioRender.com.