{"id":202946,"date":"2025-01-01T23:27:44","date_gmt":"2025-01-02T05:27:44","guid":{"rendered":"https:\/\/lifeboat.com\/blog\/2025\/01\/adipose-tissue-retains-an-epigenetic-memory-of-obesity-after-weight-loss"},"modified":"2025-01-01T23:27:44","modified_gmt":"2025-01-02T05:27:44","slug":"adipose-tissue-retains-an-epigenetic-memory-of-obesity-after-weight-loss","status":"publish","type":"post","link":"https:\/\/lifeboat.com\/blog\/2025\/01\/adipose-tissue-retains-an-epigenetic-memory-of-obesity-after-weight-loss","title":{"rendered":"Adipose tissue retains an epigenetic memory of obesity after weight loss"},"content":{"rendered":"<p><a class=\"aligncenter blog-photo\" href=\"https:\/\/lifeboat.com\/blog.images\/adipose-tissue-retains-an-epigenetic-memory-of-obesity-after-weight-loss.jpg\"><\/a><\/p>\n<p>We termed enhancers that gained (and maintained) H3K4me1 in obesity and WL \u2018new enhancers\u2019. Most of these \u2018new enhancers\u2019 were also active (that is, marked by H3K27ac) during obesity and\/or WL (Fig. <a data-track=\"click\" data-track-label=\"link\" data-track-action=\"figure anchor\" href=\"https:\/\/www.nature.com\/articles\/s41586-024-08165-7#Fig4\">4D<\/a>). We then annotated the enhancers to their closest gene and performed a GSEA. In agreement with the promoter GSEA above, we found that the \u2018new active enhancers\u2019 were related to inflammatory signalling, lysosome activity and extracellular matrix remodelling (Fig. <a data-track=\"click\" data-track-label=\"link\" data-track-action=\"figure anchor\" href=\"https:\/\/www.nature.com\/articles\/s41586-024-08165-7#Fig4\">4e<\/a> and Extended Data Fig. <a data-track=\"click\" data-track-label=\"link\" data-track-action=\"figure anchor\" href=\"https:\/\/www.nature.com\/articles\/s41586-024-08165-7#Fig14\">9i<\/a>), indicating a persistent shift of adipocytes towards a more inflammatory and less adipogenic identity. Corroborating these results, Roh <i>et al.<\/i> had analysed H3K27ac in adipocytes of obese mice and reported impaired identity maintenance during obesity<sup><a data-track=\"click\" data-track-action=\"reference anchor\" data-track-label=\"link\" data-test=\"citation-ref\" aria-label=\"Reference 25\" title=\"Roh, H. C. et al. Adipocytes fail to maintain cellular identity during obesity due to reduced PPAR\u03b3 activity and elevated TGF\u03b2-SMAD signaling. Mol. Metab. 42, 101086 (2020).\" href=\"https:\/\/www.nature.com\/articles\/s41586-024-08165-7#ref-CR25\" id=\"ref-link-section-d236379986e1698\">25<\/a><\/sup>.<\/p>\n<p>To combine our findings regarding retained translational changes and epigenetic memory, we investigated whether epigenetic mechanisms, such as differentially marked promoters or enhancers, could explain the persistent translational obesity-associated changes after WL. Notably, 57\u201362% of downregulated and 68\u201375% of upregulated persistent translational DEGs after WL could be accounted for by one or more of the analysed epigenetic modalities (Fig. <a data-track=\"click\" data-track-label=\"link\" data-track-action=\"figure anchor\" href=\"https:\/\/www.nature.com\/articles\/s41586-024-08165-7#Fig4\">4f<\/a>). Overall, these results strongly suggest the presence of stable cellular, epigenetic and transcriptional memory in mouse adipocytes that persists after WL.<\/p>\n","protected":false},"excerpt":{"rendered":"<p>We termed enhancers that gained (and maintained) H3K4me1 in obesity and WL \u2018new enhancers\u2019. Most of these \u2018new enhancers\u2019 were also active (that is, marked by H3K27ac) during obesity and\/or WL (Fig. 4D). We then annotated the enhancers to their closest gene and performed a GSEA. In agreement with the promoter GSEA above, we found [\u2026]<\/p>\n","protected":false},"author":662,"featured_media":0,"comment_status":"open","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[11,412],"tags":[],"class_list":["post-202946","post","type-post","status-publish","format-standard","hentry","category-biotech-medical","category-genetics"],"_links":{"self":[{"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/posts\/202946","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/users\/662"}],"replies":[{"embeddable":true,"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/comments?post=202946"}],"version-history":[{"count":0,"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/posts\/202946\/revisions"}],"wp:attachment":[{"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/media?parent=202946"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/categories?post=202946"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/tags?post=202946"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}