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. 2019 Oct 22;10:4799. doi: 10.1038/s41467-019-12793-3

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© The Author(s) 2019

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 — Flow chart of findings. Maternal (F0) HFD causes molecular and behavior changes in the offspring (F1) via gametic mechanisms involving epigenetic inhibition of Bdnf expression. Both low BDNF plasma levels and insulin resistance in mothers lead to alterations of BDNF and insulin signaling in the ovaries and change the recruitment of histone acetyl-transferases (HAT) and histone deacetylases (HDAC) on the Bdnf promoters. These epigenetic modifications may be transferred from oocytes to embryo. Additional mechanisms including maternal microbiota transfer, microRNA, and cryptic maternal effects may be involved in the HFD-related intergenerational modification of Bdnf epigenetic marks. The outcome is a multi-organ inhibition of Bdnf expression leading to LTP and memory deficits. The propagation of the same epigenetic changes via male sperm is responsible for the transmission of HFD-dependent brain damage to the next generations (F2 and F3)