{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang L"],"funding":["U.S. Department of Health &amp; Human Services | NIH | National Center for Advancing Translational Sciences","NCATS NIH HHS","Roubos Family Fund in Research, Mayo Nutrition and Obesity Research program","NIDDK NIH HHS","NHGRI NIH HHS","NCI NIH HHS","U.S. Department of Health &amp; Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases"],"pagination":["9361"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11522703"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_abstract":["Obesity-induced β cell dysfunction contributes to the onset of type 2 diabetes. Nevertheless, elucidating epigenetic mechanisms underlying islet dysfunction at single cell level remains challenging. Here we profile single-nuclei RNA along with enhancer marks H3K4me1 or H3K27ac in islets from lean or obese mice. Our study identifies distinct gene signatures and enhancer states correlating with β cell dysfunction trajectory. Intriguingly, while many metabolic stress-induced genes exhibit concordant changes in both H3K4me1 and H3K27ac at their enhancers, expression changes of specific subsets are solely attributable to either H3K4me1 or H3K27ac dynamics. Remarkably, a subset of H3K4me1<sup>+</sup>H3K27ac<sup>-</sup> primed enhancers prevalent in lean β cells and occupied by FoxA2 are largely "],"journal":["Nature communications"],"pubmed_title":["Heterogeneous enhancer states orchestrate β cell responses to metabolic stress."],"pmcid":["PMC11522703"],"funding_grant_id":["R01 DK098468","R01 DK131437","UL1 TR002377","R01 CA267872","R01 HG012384","K01 DK120808","R01 DK132651","R01 DK113185"],"pubmed_authors":["Obayomi SMB","Wu J","Li Y","Sramek M","Gao P","Matveyenko AV","Wei Z","Wang L"],"additional_accession":[]},"is_claimable":false,"name":"Heterogeneous enhancer states orchestrate β cell responses to metabolic stress.","description":"Obesity-induced β cell dysfunction contributes to the onset of type 2 diabetes. Nevertheless, elucidating epigenetic mechanisms underlying islet dysfunction at single cell level remains challenging. Here we profile single-nuclei RNA along with enhancer marks H3K4me1 or H3K27ac in islets from lean or obese mice. Our study identifies distinct gene signatures and enhancer states correlating with β cell dysfunction trajectory. Intriguingly, while many metabolic stress-induced genes exhibit concordant changes in both H3K4me1 and H3K27ac at their enhancers, expression changes of specific subsets are solely attributable to either H3K4me1 or H3K27ac dynamics. Remarkably, a subset of H3K4me1<sup>+</sup>H3K27ac<sup>-</sup> primed enhancers prevalent in lean β cells and occupied by FoxA2 are largely ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Oct","modification":"2026-07-16T03:08:31.391Z","creation":"2025-04-04T02:34:21.03Z"},"accession":"S-EPMC11522703","cross_references":{"pubmed":["39472434"],"doi":["10.1038/s41467-024-53717-0"]}}