{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:52:35Z","timestamp":1792788755116,"version":"4.5.0"},"reference-count":57,"publisher":"American Diabetes Association","issue":"11","license":[{"start":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T00:00:00Z","timestamp":1789430400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.diabetesjournals.org\/journals\/pages\/license"}],"funder":[{"name":"International Science and Technology Cooperation Project of the Science and Technology Department of Jilin Province","award":["20230402002GH"],"award-info":[{"award-number":["20230402002GH"]}]},{"name":"Norman Bethune Foundations of Jilin University","award":["2024JBGS09"],"award-info":[{"award-number":["2024JBGS09"]}],"id":[{"id":"https:\/\/ror.org\/00js3aw79","id-type":"ROR","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82170369"],"award-info":[{"award-number":["82170369"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82370373"],"award-info":[{"award-number":["82370373"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,11,1]]},"abstract":"<jats:sec>\n                    <jats:title\/>\n                    <jats:p>Abnormal iron metabolism and ferroptosis contribute to diabetic cardiomyopathy (DCM); however, the regulatory mechanisms remain unclear. Inulin improves systemic metabolism and cardiac function, but whether it alleviates myocardial ferroptosis and DCM is unknown. Using two distinct type 2 diabetes (T2D) mouse models\u2014the high-fat diet combined with streptozotocin\u2013induced T2D model and the db\/db mouse model\u2014in combination with an iron chelator, we found that imbalanced iron homeostasis and ferroptosis drive DCM. Inulin restored cardiac iron homeostasis, inhibited ferroptosis and DCM, and promoted short-chain fatty acids (SCFAs). Treatment with an SCFA inhibitor confirmed that SCFAs mediate the cardioprotective effects of inulin, with butyrate exerting the most potent antiferroptotic effect. Hypoxia-inducible factor 1\u03b1 (HIF-1\u03b1) expression was decreased in DCM, and bioinformatic analysis identified HIF-1\u03b1 as a hub gene in ferroptosis. Interference with HIF-1\u03b1 in the two distinct T2D mouse models and in\u00a0vitro weakened the antiferroptotic effect of butyrate. Mechanistically, butyrate inhibited HIF-1\u03b1 ubiquitination by inducing HIF-1\u03b1 butyrylation at lysine 190, which upregulated transcription of ferritin heavy chain (FTH) and mitochondrial ferritin (FTMT) to enhance the storage of unstable iron. HIF-1\u03b1 acts as a critical regulator of myocardial iron homeostasis through transcriptional upregulation of FTH\/FTMT. Inulin-fermented butyrate prevents ferroptosis-driven DCM, and its protective effect depends on the HIF-1\u03b1\u2013FTH\/FTMT axis via butyrylation. These findings highlight the therapeutic potential of using inulin or targeting HIF-1\u03b1 in the management of DCM and diseases associated with aberrant iron metabolism.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Article Highlights<\/jats:title>\n                    <jats:p>Dysregulated iron metabolism and ferroptosis contribute to diabetic cardiomyopathy (DCM); however, the regulatory mechanisms and effective therapeutic strategies remain elusive. We sought to identify the role of hypoxia-inducible factor 1\u03b1 (HIF-1\u03b1) in regulating myocardial iron homeostasis and ferroptosis in DCM, as well as evaluate the preventive effects of inulin on ferroptosis-induced DCM and elucidate its mechanism. Inulin-fermented butyrate activates the HIF-1\u03b1\u2013ferritin heavy chain (FTH)\/mitochondrial ferritin (FTMT) axis, alleviating cardiac ferroptosis and DCM, and stabilizes HIF-1\u03b1 by promoting K190 Kbu modification and inhibiting ubiquitin-dependent degradation. Targeting the HIF-1\u03b1\u2013FTH\/FTMT axis via inulin, butyrate, or alternative approaches may represent a promising therapeutic strategy for alleviating DCM and other diabetes complications.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2337\/db26-0063","type":"journal-article","created":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T17:01:27Z","timestamp":1789491687000},"page":"2076-2093","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":0,"title":["Inulin- and Butyrate-Mediated HIF-1\u03b1 Butyrylation Prevent Diabetic Ferroptosis and Cardiomyopathy by Maintaining Iron Homeostasis"],"prefix":"10.2337","volume":"75","author":[{"given":"Ge","family":"Yang","sequence":"first","affiliation":[{"name":"Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University 1 , Changchun, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9489-7386","authenticated-orcid":false,"given":"Yuan","family":"Tian","sequence":"additional","affiliation":[{"name":"Department of Gynecology and Obstetrics, Second Hospital of Jilin University 2 , Changchun, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rui","family":"Sun","sequence":"additional","affiliation":[{"name":"Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University 1 , Changchun, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chao","family":"Dong","sequence":"additional","affiliation":[{"name":"Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University 1 , Changchun, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanru","family":"Li","sequence":"additional","affiliation":[{"name":"Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University 1 , Changchun, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuang","family":"Li","sequence":"additional","affiliation":[{"name":"Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University 1 , Changchun, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haiying","family":"Zhang","sequence":"additional","affiliation":[{"name":"Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University 1 , Changchun, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7591-9423","authenticated-orcid":false,"given":"Ying","family":"Xin","sequence":"additional","affiliation":[{"name":"Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University 1 , Changchun, 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