{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T13:41:58Z","timestamp":1789998118707,"version":"4.0.1"},"reference-count":80,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2025,10,24]],"date-time":"2025-10-24T00:00:00Z","timestamp":1761264000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2025,10,24]],"date-time":"2025-10-24T00:00:00Z","timestamp":1761264000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"funder":[{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["MO 2774\/6-1 project number 505680640"],"award-info":[{"award-number":["MO 2774\/6-1 project number 505680640"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["MO 2774\/7-1 project number: 508372800"],"award-info":[{"award-number":["MO 2774\/7-1 project number: 508372800"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["TRR 219 Project ID 322900939"],"award-info":[{"award-number":["TRR 219 Project ID 322900939"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100005690","name":"Universit\u00e4t des Saarlandes","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100005690","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Diabetologia"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims\/hypothesis<\/jats:title>\n                    <jats:p>\n                      Barth syndrome is a mitochondrial disorder caused by\n                      <jats:italic>Tafazzin<\/jats:italic>\n                      (\n                      <jats:italic>TAZ<\/jats:italic>\n                      ) mutations, which impair cardiolipin remodelling and contribute to systemic metabolic alterations. While islet dysfunction has been implicated in Barth syndrome, its underlying mechanisms remain unknown. We aimed to determine how Tafazzin (Taz) deficiency affects mouse pancreatic islet metabolism and hormone secretion, and whether systemic signals, such as circulating factors, modulate these effects in vivo. In vivo and in vitro models were used to separate direct islet effects from systemic influences of Taz deficiency.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We used a mouse model of global\n                      <jats:italic>Taz<\/jats:italic>\n                      knockdown (\n                      <jats:italic>Taz<\/jats:italic>\n                      -KD) and combined in vivo and in vitro approaches to assess pancreatic islet metabolism, morphology and hormone secretion. Islet function was evaluated under basal and glucotoxic conditions. Transcriptomic profiling was performed to identify gene expression changes in isolated islets from\n                      <jats:italic>Taz<\/jats:italic>\n                      -KD mice and following in vitro\n                      <jats:italic>Taz<\/jats:italic>\n                      -KD. Additionally, we examined the role of the circulating factor fibroblast growth factor 21 (FGF-21) in modulating islet function.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Despite impaired cardiolipin remodelling, pancreatic islets from\n                      <jats:italic>Taz<\/jats:italic>\n                      -KD mice maintained insulin secretion, supported by compensatory mechanisms such as increased glucose uptake, expanded mitochondrial volume and increased metabolic parameters. In addition, alpha cell mass and glucagon secretion were significantly increased in\n                      <jats:italic>Taz<\/jats:italic>\n                      -KD islets. These islet-specific adaptations occurred alongside improved whole-body glucose tolerance, elevated circulating FGF-21 levels and enhanced glucose uptake in brown adipose tissue. In contrast, in vitro\n                      <jats:italic>Taz<\/jats:italic>\n                      -KD led to impaired islet function and reduced insulin secretion. Transcriptomic analysis revealed distinct gene expression patterns between in vivo and in vitro\n                      <jats:italic>Taz<\/jats:italic>\n                      -KD models. While in vivo upregulation of genes related to\n                      <jats:italic>N<\/jats:italic>\n                      -acetylglucosamine biosynthesis and\n                      <jats:italic>O<\/jats:italic>\n                      -GlcNAcylation were related to compensatory mechanisms, in vitro\n                      <jats:italic>Taz<\/jats:italic>\n                      -KD affected, among others, the MAPK pathway, contributing to islet dysfunction. Notably, islet incubation with FGF-21 was able to restore insulin secretion after in vitro\n                      <jats:italic>Taz<\/jats:italic>\n                      -KD.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions\/interpretation<\/jats:title>\n                    <jats:p>\n                      Our findings demonstrate that while\n                      <jats:italic>Taz<\/jats:italic>\n                      and cardiolipin remodelling are essential for beta cell physiology, systemic and islet-specific compensatory mechanisms preserve insulin secretion in vivo in\n                      <jats:italic>Taz<\/jats:italic>\n                      -KD mice, alongside increased glucagon secretion. These adaptations probably contribute to the altered metabolic phenotype observed in Barth syndrome and highlight a potential role for hormones and circulating factors such as FGF-21 in maintaining islet function and glucose homeostasis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Graphical Abstract<\/jats:title>\n                  <\/jats:sec>","DOI":"10.1007\/s00125-025-06575-4","type":"journal-article","created":{"date-parts":[[2025,10,24]],"date-time":"2025-10-24T15:46:25Z","timestamp":1761320785000},"page":"173-197","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Adaptive mechanisms in pancreatic islets counteract mitochondrial dysfunction in Barth syndrome"],"prefix":"10.1007","volume":"69","author":[{"given":"Christopher","family":"Carlein","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Markus D. A.","family":"Hoffmann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Caroline","family":"Bickelmann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andressa G.","family":"Amaral","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ahmadali","family":"Lotfinia","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laurie-Anne","family":"de Selliers","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johanne","family":"Audouze-Chaud","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Selina","family":"Wrublewsky","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcel A.","family":"Lauterbach","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karina","family":"von der Malsburg","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"van der Laan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Monika","family":"Bozem","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Markus","family":"Hoth","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrick","family":"Gilon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Magalie A.","family":"Ravier","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruce","family":"Morgan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emmanuel","family":"Ampofo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takahiro","family":"Higuchi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edoardo","family":"Bertero","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jan","family":"Dudek","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christoph","family":"Maack","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leticia Prates","family":"Roma","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,10,24]]},"reference":[{"issue":"4","key":"6575_CR1","doi-asserted-by":"publisher","first-page":"399","DOI":"10.1093\/cvr\/cvx014","volume":"113","author":"J Dudek","year":"2017","unstructured":"Dudek J, Maack C (2017) Barth syndrome cardiomyopathy. Cardiovasc Res 113(4):399\u2013410. https:\/\/doi.org\/10.1093\/cvr\/cvx014","journal-title":"Cardiovasc Res"},{"issue":"3","key":"6575_CR2","doi-asserted-by":"publisher","first-page":"e0151802","DOI":"10.1371\/journal.pone.0151802","volume":"11","author":"Y Sandlers","year":"2016","unstructured":"Sandlers Y, Mercier K, Pathmasiri W et al (2016) Metabolomics reveals new mechanisms for pathogenesis in barth syndrome and introduces novel roles for cardiolipin in cellular function. PLoS One 11(3):e0151802. https:\/\/doi.org\/10.1371\/journal.pone.0151802","journal-title":"PLoS One"},{"issue":"3","key":"6575_CR3","doi-asserted-by":"publisher","first-page":"993","DOI":"10.1042\/BST20190932","volume":"48","author":"AL Duncan","year":"2020","unstructured":"Duncan AL (2020) Monolysocardiolipin (MLCL) interactions with mitochondrial membrane proteins. Biochem Soc Trans 48(3):993\u20131004. https:\/\/doi.org\/10.1042\/BST20190932","journal-title":"Biochem Soc Trans"},{"issue":"45","key":"6575_CR4","doi-asserted-by":"publisher","first-page":"13489","DOI":"10.1039\/d2sc04072g","volume":"13","author":"RA Corey","year":"2022","unstructured":"Corey RA, Harrison N, Stansfeld PJ, Sansom MSP, Duncan AL (2022) Cardiolipin, and not monolysocardiolipin, preferentially binds to the interface of complexes III and IV. Chem Sci 13(45):13489\u201313498. https:\/\/doi.org\/10.1039\/d2sc04072g","journal-title":"Chem Sci"},{"issue":"1","key":"6575_CR5","doi-asserted-by":"publisher","first-page":"17","DOI":"10.1002\/jimd.12453","volume":"45","author":"R Thompson","year":"2022","unstructured":"Thompson R, Jefferies J, Wang S et al (2022) Current and future treatment approaches for Barth syndrome. J Inherit Metab Dis 45(1):17\u201328. https:\/\/doi.org\/10.1002\/jimd.12453","journal-title":"J Inherit Metab Dis"},{"key":"6575_CR6","doi-asserted-by":"publisher","first-page":"915301","DOI":"10.3389\/fmolb.2022.915301","volume":"9","author":"Z Liang","year":"2022","unstructured":"Liang Z, Schmidtke MW, Greenberg ML (2022) Current knowledge on the role of cardiolipin remodeling in the context of lipid oxidation and Barth syndrome. Front Mol Biosci 9:915301. https:\/\/doi.org\/10.3389\/fmolb.2022.915301","journal-title":"Front Mol Biosci"},{"issue":"1","key":"6575_CR7","doi-asserted-by":"publisher","first-page":"82","DOI":"10.1002\/jimd.12427","volume":"45","author":"J Dudek","year":"2022","unstructured":"Dudek J, Maack C (2022) Mechano-energetic aspects of Barth syndrome. J Inherit Metab Dis 45(1):82\u201398. https:\/\/doi.org\/10.1002\/jimd.12427","journal-title":"J Inherit Metab Dis"},{"issue":"9","key":"6575_CR8","doi-asserted-by":"publisher","first-page":"2134","DOI":"10.1080\/15548627.2021.2020979","volume":"18","author":"J Zhang","year":"2022","unstructured":"Zhang J, Liu X, Nie J, Shi Y (2022) Restoration of mitophagy ameliorates cardiomyopathy in Barth syndrome. Autophagy 18(9):2134\u20132149. https:\/\/doi.org\/10.1080\/15548627.2021.2020979","journal-title":"Autophagy"},{"issue":"21","key":"6575_CR9","doi-asserted-by":"publisher","first-page":"1694","DOI":"10.1161\/CIRCULATIONAHA.121.053755","volume":"144","author":"E Bertero","year":"2021","unstructured":"Bertero E, Nickel A, Kohlhaas M et al (2021) Loss of mitochondrial Ca(2+) uniporter limits inotropic reserve and provides trigger and substrate for arrhythmias in Barth syndrome cardiomyopathy. Circulation 144(21):1694\u20131713. https:\/\/doi.org\/10.1161\/CIRCULATIONAHA.121.053755","journal-title":"Circulation"},{"issue":"9","key":"6575_CR10","doi-asserted-by":"publisher","first-page":"e17399","DOI":"10.15252\/emmm.202317399","volume":"15","author":"A Chowdhury","year":"2023","unstructured":"Chowdhury A, Boshnakovska A, Aich A et al (2023) Metabolic switch from fatty acid oxidation to glycolysis in knock-in mouse model of Barth syndrome. EMBO Mol Med 15(9):e17399. https:\/\/doi.org\/10.15252\/emmm.202317399","journal-title":"EMBO Mol Med"},{"issue":"8","key":"6575_CR11","doi-asserted-by":"publisher","first-page":"e0290832","DOI":"10.1371\/journal.pone.0290832","volume":"18","author":"GG Schweitzer","year":"2023","unstructured":"Schweitzer GG, Ditzenberger GL, Hughey CC et al (2023) Elevated liver glycogenolysis mediates higher blood glucose during acute exercise in Barth syndrome. PLoS One 18(8):e0290832. https:\/\/doi.org\/10.1371\/journal.pone.0290832","journal-title":"PLoS One"},{"issue":"10","key":"6575_CR12","doi-asserted-by":"publisher","first-page":"2333","DOI":"10.3390\/cells9102333","volume":"9","author":"PX Petit","year":"2020","unstructured":"Petit PX, Ardilla-Osorio H, Penalvia L, Rainey NE (2020) Tafazzin Mutation Affecting Cardiolipin Leads to Increased Mitochondrial Superoxide Anions and Mitophagy Inhibition in Barth Syndrome. Cells 9(10):2333. https:\/\/doi.org\/10.3390\/cells9102333","journal-title":"Cells"},{"key":"6575_CR13","doi-asserted-by":"publisher","first-page":"158542","DOI":"10.1016\/j.bbalip.2019.158542","volume":"2","author":"VA Patil","year":"2020","unstructured":"Patil VA, Li Y, Ji J, Greenberg ML (2020) Loss of the mitochondrial lipid cardiolipin leads to decreased glutathione synthesis. Biochim Biophys Acta Mol Cell Biol Lipids 2:158542. https:\/\/doi.org\/10.1016\/j.bbalip.2019.158542","journal-title":"Biochim Biophys Acta Mol Cell Biol Lipids"},{"key":"6575_CR14","doi-asserted-by":"publisher","first-page":"654198","DOI":"10.1155\/2014\/654198","volume":"2014","author":"Q He","year":"2014","unstructured":"He Q, Harris N, Ren J, Han X (2014) Mitochondria-targeted antioxidant prevents cardiac dysfunction induced by tafazzin gene knockdown in cardiac myocytes. Oxid Med Cell Longev 2014:654198. https:\/\/doi.org\/10.1155\/2014\/654198","journal-title":"Oxid Med Cell Longev"},{"issue":"1","key":"6575_CR15","doi-asserted-by":"publisher","first-page":"47","DOI":"10.1007\/s00395-023-01017-x","volume":"118","author":"I Kutschka","year":"2023","unstructured":"Kutschka I, Bertero E, Wasmus C et al (2023) Activation of the integrated stress response rewires cardiac metabolism in Barth syndrome. Basic Res Cardiol 118(1):47. https:\/\/doi.org\/10.1007\/s00395-023-01017-x","journal-title":"Basic Res Cardiol"},{"issue":"50","key":"6575_CR16","doi-asserted-by":"publisher","first-page":"16684","DOI":"10.1021\/bi051908a","volume":"44","author":"X Han","year":"2005","unstructured":"Han X, Yang J, Cheng H, Yang K, Abendschein DR, Gross RW (2005) Shotgun lipidomics identifies cardiolipin depletion in diabetic myocardium linking altered substrate utilization with mitochondrial dysfunction. Biochemistry 44(50):16684\u201316694. https:\/\/doi.org\/10.1021\/bi051908a","journal-title":"Biochemistry"},{"issue":"21","key":"6575_CR17","doi-asserted-by":"publisher","first-page":"6417","DOI":"10.1021\/bi7004015","volume":"46","author":"X Han","year":"2007","unstructured":"Han X, Yang J, Yang K, Zhao Z, Abendschein DR, Gross RW (2007) Alterations in myocardial cardiolipin content and composition occur at the very earliest stages of diabetes: a shotgun lipidomics study. Biochemistry 46(21):6417\u20136428. https:\/\/doi.org\/10.1021\/bi7004015","journal-title":"Biochemistry"},{"issue":"1","key":"6575_CR18","doi-asserted-by":"publisher","first-page":"159","DOI":"10.1016\/j.cmet.2018.05.003","volume":"28","author":"EG Sustarsic","year":"2018","unstructured":"Sustarsic EG, Ma T, Lynes MD et al (2018) Cardiolipin synthesis in brown and beige fat mitochondria is essential for systemic energy homeostasis. Cell Metab 28(1):159\u2013174 e111. https:\/\/doi.org\/10.1016\/j.cmet.2018.05.003","journal-title":"Cell Metab"},{"issue":"11","key":"6575_CR19","doi-asserted-by":"publisher","first-page":"3289","DOI":"10.2337\/db16-0114","volume":"65","author":"LK Cole","year":"2016","unstructured":"Cole LK, Mejia EM, Vandel M et al (2016) Impaired cardiolipin biosynthesis prevents hepatic steatosis and diet-induced obesity. Diabetes 65(11):3289\u20133300. https:\/\/doi.org\/10.2337\/db16-0114","journal-title":"Diabetes"},{"issue":"2","key":"6575_CR20","doi-asserted-by":"publisher","first-page":"58","DOI":"10.29245\/2572-9411\/2017\/2.1087","volume":"2","author":"V Raja","year":"2017","unstructured":"Raja V, Reynolds CA, Greenberg ML (2017) Barth syndrome: a life-threatening disorder caused by abnormal cardiolipin remodeling. J Rare Dis Res Treat 2(2):58\u201362. https:\/\/doi.org\/10.29245\/2572-9411\/2017\/2.1087","journal-title":"J Rare Dis Res Treat"},{"issue":"5","key":"6575_CR21","doi-asserted-by":"publisher","first-page":"684","DOI":"10.1007\/s10545-006-0388-7","volume":"29","author":"MA Donati","year":"2006","unstructured":"Donati MA, Malvagia S, Pasquini E et al (2006) Barth syndrome presenting with acute metabolic decompensation in the neonatal period. J Inherit Metab Dis 29(5):684. https:\/\/doi.org\/10.1007\/s10545-006-0388-7","journal-title":"J Inherit Metab Dis"},{"issue":"1","key":"6575_CR22","doi-asserted-by":"publisher","first-page":"91","DOI":"10.1007\/s10545-012-9486-x","volume":"36","author":"WT Cade","year":"2013","unstructured":"Cade WT, Spencer CT, Reeds DN et al (2013) Substrate metabolism during basal and hyperinsulinemic conditions in adolescents and young-adults with Barth syndrome. J Inherit Metab Dis 36(1):91\u2013101. https:\/\/doi.org\/10.1007\/s10545-012-9486-x","journal-title":"J Inherit Metab Dis"},{"issue":"7","key":"6575_CR23","doi-asserted-by":"publisher","first-page":"bqab102","DOI":"10.1210\/endocr\/bqab102","volume":"162","author":"LK Cole","year":"2021","unstructured":"Cole LK, Agarwal P, Doucette CA et al (2021) Tafazzin deficiency reduces basal insulin secretion and mitochondrial function in pancreatic islets from male mice. Endocrinology 162(7):bqab102. https:\/\/doi.org\/10.1210\/endocr\/bqab102","journal-title":"Endocrinology"},{"issue":"2","key":"6575_CR24","doi-asserted-by":"publisher","first-page":"899","DOI":"10.1074\/jbc.M110.171439","volume":"286","author":"D Acehan","year":"2011","unstructured":"Acehan D, Vaz F, Houtkooper RH et al (2011) Cardiac and skeletal muscle defects in a mouse model of human Barth syndrome. J Biol Chem 286(2):899\u2013908. https:\/\/doi.org\/10.1074\/jbc.M110.171439","journal-title":"J Biol Chem"},{"issue":"419","key":"6575_CR25","doi-asserted-by":"publisher","first-page":"rs1","DOI":"10.1126\/scisignal.aad3895","volume":"9","author":"Y Fujikawa","year":"2016","unstructured":"Fujikawa Y, Roma LP, Sobotta MC et al (2016) Mouse redox histology using genetically encoded probes. Sci Signal 9(419):rs1. https:\/\/doi.org\/10.1126\/scisignal.aad3895","journal-title":"Sci Signal"},{"issue":"4","key":"6575_CR26","doi-asserted-by":"publisher","first-page":"545","DOI":"10.3748\/wjg.v11.i4.545","volume":"11","author":"YF Cui","year":"2005","unstructured":"Cui YF, Ma M, Wang GY, Han DE, Vollmar B, Menger MD (2005) Prevention of core cell damage in isolated islets of Langerhans by low temperature preconditioning. World J Gastroenterol 11(4):545\u2013550. https:\/\/doi.org\/10.3748\/wjg.v11.i4.545","journal-title":"World J Gastroenterol"},{"issue":"8","key":"6575_CR27","doi-asserted-by":"publisher","first-page":"2226","DOI":"10.1007\/s00125-012-2581-6","volume":"55","author":"LP Roma","year":"2012","unstructured":"Roma LP, Pascal SM, Duprez J, Jonas JC (2012) Mitochondrial oxidative stress contributes differently to rat pancreatic islet cell apoptosis and insulin secretory defects after prolonged culture in a low non-stimulating glucose concentration. Diabetologia 55(8):2226\u20132237. https:\/\/doi.org\/10.1007\/s00125-012-2581-6","journal-title":"Diabetologia"},{"issue":"1","key":"6575_CR28","doi-asserted-by":"publisher","first-page":"334","DOI":"10.1038\/s41467-023-44589-x","volume":"15","author":"H Lin","year":"2024","unstructured":"Lin H, Suzuki K, Smith N et al (2024) A role and mechanism for redox sensing by SENP1 in \u03b2-cell responses to high fat feeding. Nat Commun 15(1):334. https:\/\/doi.org\/10.1038\/s41467-023-44589-x","journal-title":"Nat Commun"},{"key":"6575_CR29","doi-asserted-by":"publisher","first-page":"104895","DOI":"10.1016\/j.yexmp.2024.104895","volume":"137","author":"E Vianello","year":"2024","unstructured":"Vianello E, Ambrogi F, Kalousova M et al (2024) Circulating perturbation of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) is associated to cardiac remodeling and NLRP3 inflammasome in cardiovascular patients with insulin resistance risk. Exp Mol Pathol 137:104895. https:\/\/doi.org\/10.1016\/j.yexmp.2024.104895","journal-title":"Exp Mol Pathol"},{"issue":"5","key":"6575_CR30","doi-asserted-by":"publisher","first-page":"969","DOI":"10.2337\/db11-1564","volume":"61","author":"F Schuit","year":"2012","unstructured":"Schuit F, Van Lommel L, Granvik M et al (2012) \u03b2-cell-specific gene repression: a mechanism to protect against inappropriate or maladjusted insulin secretion? Diabetes 61(5):969\u2013975. https:\/\/doi.org\/10.2337\/db11-1564","journal-title":"Diabetes"},{"issue":"7","key":"6575_CR31","doi-asserted-by":"publisher","first-page":"4895","DOI":"10.1016\/S0021-9258(17)37629-9","volume":"269","author":"N Sekine","year":"1994","unstructured":"Sekine N, Cirulli V, Regazzi R et al (1994) Low lactate dehydrogenase and high mitochondrial glycerol phosphate dehydrogenase in pancreatic beta-cells. Potential role in nutrient sensing. J Biol Chem 269(7):4895\u20134902","journal-title":"J Biol Chem"},{"issue":"3","key":"6575_CR32","doi-asserted-by":"publisher","first-page":"415","DOI":"10.1002\/1873-3468.13973","volume":"595","author":"RLS Goncalves","year":"2021","unstructured":"Goncalves RLS, Schlame M, Bartelt A, Brand MD, Hotamisligil GS (2021) Cardiolipin deficiency in Barth syndrome is not associated with increased superoxide\/H(2) O(2) production in heart and skeletal muscle mitochondria. FEBS Lett 595(3):415\u2013432. https:\/\/doi.org\/10.1002\/1873-3468.13973","journal-title":"FEBS Lett"},{"issue":"8","key":"6575_CR33","doi-asserted-by":"publisher","first-page":"1929","DOI":"10.1016\/j.bbagen.2017.05.013","volume":"1861","author":"S Lenzen","year":"2017","unstructured":"Lenzen S (2017) Chemistry and biology of reactive species with special reference to the antioxidative defence status in pancreatic \u03b2-cells. Biochim Biophys Acta Gen Subj 1861(8):1929\u20131942. https:\/\/doi.org\/10.1016\/j.bbagen.2017.05.013","journal-title":"Biochim Biophys Acta Gen Subj"},{"issue":"7","key":"6575_CR34","doi-asserted-by":"publisher","first-page":"1783","DOI":"10.2337\/db06-1601","volume":"56","author":"J Pi","year":"2007","unstructured":"Pi J, Bai Y, Zhang Q et al (2007) Reactive oxygen species as a signal in glucose-stimulated insulin secretion. Diabetes 56(7):1783\u20131791. https:\/\/doi.org\/10.2337\/db06-1601","journal-title":"Diabetes"},{"issue":"7","key":"6575_CR35","doi-asserted-by":"publisher","first-page":"1341","DOI":"10.2337\/db19-1130","volume":"69","author":"L Plecita-Hlavata","year":"2020","unstructured":"Plecita-Hlavata L, Jaburek M, Holendova B et al (2020) Glucose-stimulated insulin secretion fundamentally requires H(2)O(2) signaling by NADPH oxidase 4. Diabetes 69(7):1341\u20131354. https:\/\/doi.org\/10.2337\/db19-1130","journal-title":"Diabetes"},{"issue":"12","key":"6575_CR36","doi-asserted-by":"publisher","first-page":"1035","DOI":"10.1016\/j.tibs.2016.09.001","volume":"41","author":"A Raffaello","year":"2016","unstructured":"Raffaello A, Mammucari C, Gherardi G, Rizzuto R (2016) Calcium at the center of cell signaling: interplay between endoplasmic reticulum, mitochondria, and lysosomes. Trends Biochem Sci 41(12):1035\u20131049. https:\/\/doi.org\/10.1016\/j.tibs.2016.09.001","journal-title":"Trends Biochem Sci"},{"issue":"5","key":"6575_CR37","doi-asserted-by":"publisher","first-page":"340","DOI":"10.1016\/j.ceca.2014.09.001","volume":"56","author":"P Gilon","year":"2014","unstructured":"Gilon P, Chae HY, Rutter GA, Ravier MA (2014) Calcium signaling in pancreatic \u03b2-cells in health and in Type 2 diabetes. Cell Calcium 56(5):340\u2013361. https:\/\/doi.org\/10.1016\/j.ceca.2014.09.001","journal-title":"Cell Calcium"},{"issue":"10","key":"6575_CR38","doi-asserted-by":"publisher","first-page":"2533","DOI":"10.2337\/db10-1543","volume":"60","author":"MA Ravier","year":"2011","unstructured":"Ravier MA, Daro D, Roma LP et al (2011) Mechanisms of control of the free Ca2+ concentration in the endoplasmic reticulum of mouse pancreatic \u03b2-cells: interplay with cell metabolism and [Ca2+]c and role of SERCA2b and SERCA3. Diabetes 60(10):2533\u20132545. https:\/\/doi.org\/10.2337\/db10-1543","journal-title":"Diabetes"},{"issue":"Suppl","key":"6575_CR39","doi-asserted-by":"publisher","first-page":"54","DOI":"10.1002\/jcb.240550007","volume":"55","author":"FM Ashcroft","year":"1994","unstructured":"Ashcroft FM, Proks P, Smith PA, Ammala C, Bokvist K, Rorsman P (1994) Stimulus-secretion coupling in pancreatic \u03b2 cells. J Cell Biochem 55(Suppl):54\u201365. https:\/\/doi.org\/10.1002\/jcb.240550007","journal-title":"J Cell Biochem"},{"issue":"10","key":"6575_CR40","doi-asserted-by":"publisher","first-page":"2064","DOI":"10.1007\/s00125-020-05196-3","volume":"63","author":"T Moede","year":"2020","unstructured":"Moede T, Leibiger IB, Berggren PO (2020) Alpha cell regulation of beta cell function. Diabetologia 63(10):2064\u20132075. https:\/\/doi.org\/10.1007\/s00125-020-05196-3","journal-title":"Diabetologia"},{"issue":"3","key":"6575_CR41","doi-asserted-by":"publisher","first-page":"428","DOI":"10.1093\/hmg\/ddn370","volume":"18","author":"V Serre-Beinier","year":"2009","unstructured":"Serre-Beinier V, Bosco D, Zulianello L et al (2009) Cx36 makes channels coupling human pancreatic \u03b2-cells, and correlates with insulin expression. Hum Mol Genet 18(3):428\u2013439. https:\/\/doi.org\/10.1093\/hmg\/ddn370","journal-title":"Hum Mol Genet"},{"issue":"4","key":"6575_CR42","doi-asserted-by":"publisher","first-page":"643","DOI":"10.1080\/15548627.2015.1023984","volume":"11","author":"P Hsu","year":"2015","unstructured":"Hsu P, Liu X, Zhang J, Wang HG, Ye JM, Shi Y (2015) Cardiolipin remodeling by TAZ\/tafazzin is selectively required for the initiation of mitophagy. Autophagy 11(4):643\u2013652. https:\/\/doi.org\/10.1080\/15548627.2015.1023984","journal-title":"Autophagy"},{"issue":"1","key":"6575_CR43","doi-asserted-by":"publisher","first-page":"13655","DOI":"10.1038\/s41598-024-64368-y","volume":"14","author":"S Russo","year":"2024","unstructured":"Russo S, De Rasmo D, Rossi R, Signorile A, Lobasso S (2024) SS-31 treatment ameliorates cardiac mitochondrial morphology and defective mitophagy in a murine model of Barth syndrome. Sci Rep 14(1):13655. https:\/\/doi.org\/10.1038\/s41598-024-64368-y","journal-title":"Sci Rep"},{"issue":"3","key":"6575_CR44","doi-asserted-by":"publisher","first-page":"107676","DOI":"10.1016\/j.ymgme.2023.107676","volume":"140","author":"O Liu","year":"2023","unstructured":"Liu O, Chinni BK, Manlhiot C, Vernon HJ (2023) FGF21 and GDF15 are elevated in Barth Syndrome and are correlated to important clinical measures. Mol Genet Metab 140(3):107676. https:\/\/doi.org\/10.1016\/j.ymgme.2023.107676","journal-title":"Mol Genet Metab"},{"key":"6575_CR45","doi-asserted-by":"publisher","first-page":"23","DOI":"10.1186\/1750-1172-8-23","volume":"8","author":"SL Clarke","year":"2013","unstructured":"Clarke SL, Bowron A, Gonzalez IL et al (2013) Barth syndrome. Orphanet J Rare Dis 8:23. https:\/\/doi.org\/10.1186\/1750-1172-8-23","journal-title":"Orphanet J Rare Dis"},{"issue":"7","key":"6575_CR46","doi-asserted-by":"publisher","first-page":"1533","DOI":"10.7150\/ijbs.32020","volume":"15","author":"J Li","year":"2019","unstructured":"Li J, Du H, Zhang M et al (2019) Amorphous solid dispersion of Berberine mitigates apoptosis via iPLA(2)\u03b2\/Cardiolipin\/Opa1 pathway in db\/db mice and in Palmitate-treated MIN6 \u03b2-cells. Int J Biol Sci 15(7):1533\u20131545. https:\/\/doi.org\/10.7150\/ijbs.32020","journal-title":"Int J Biol Sci"},{"issue":"20","key":"6575_CR47","doi-asserted-by":"publisher","first-page":"14194","DOI":"10.1074\/jbc.M114.561910","volume":"289","author":"H Song","year":"2014","unstructured":"Song H, Wohltmann M, Tan M, Ladenson JH, Turk J (2014) Group VIA phospholipase A2 mitigates palmitate-induced \u03b2-cell mitochondrial injury and apoptosis. J Biol Chem 289(20):14194\u201314210. https:\/\/doi.org\/10.1074\/jbc.M114.561910","journal-title":"J Biol Chem"},{"issue":"12","key":"6575_CR48","doi-asserted-by":"publisher","first-page":"e0271651","DOI":"10.1371\/journal.pone.0271651","volume":"17","author":"S Nemoto","year":"2022","unstructured":"Nemoto S, Kubota T, Ohno H (2022) Metabolic differences and differentially expressed genes between C57BL\/6J and C57BL\/6N mice substrains. PLoS One 17(12):e0271651. https:\/\/doi.org\/10.1371\/journal.pone.0271651","journal-title":"PLoS One"},{"issue":"11","key":"6575_CR49","doi-asserted-by":"publisher","first-page":"2550","DOI":"10.1007\/s00125-021-05548-7","volume":"64","author":"AF Close","year":"2021","unstructured":"Close AF, Chae H, Jonas JC (2021) The lack of functional nicotinamide nucleotide transhydrogenase only moderately contributes to the impairment of glucose tolerance and glucose-stimulated insulin secretion in C57BL\/6J vs C57BL\/6N mice. Diabetologia 64(11):2550\u20132561. https:\/\/doi.org\/10.1007\/s00125-021-05548-7","journal-title":"Diabetologia"},{"issue":"6","key":"6575_CR50","doi-asserted-by":"publisher","first-page":"535","DOI":"10.1016\/j.molmet.2017.04.004","volume":"6","author":"LRB Santos","year":"2017","unstructured":"Santos LRB, Muller C, de Souza AH et al (2017) NNT reverse mode of operation mediates glucose control of mitochondrial NADPH and glutathione redox state in mouse pancreatic \u03b2-cells. Mol Metab 6(6):535\u2013547. https:\/\/doi.org\/10.1016\/j.molmet.2017.04.004","journal-title":"Mol Metab"},{"issue":"5","key":"6575_CR51","doi-asserted-by":"publisher","first-page":"229","DOI":"10.1007\/s100380200030","volume":"47","author":"O Sakamoto","year":"2002","unstructured":"Sakamoto O, Kitoh T, Ohura T, Ohya N, Iinuma K (2002) Novel missense mutation (R94S) in the TAZ (G4.5) gene in a Japanese patient with Barth syndrome. J Hum Genet 47(5):229\u2013231. https:\/\/doi.org\/10.1007\/s100380200030","journal-title":"J Hum Genet"},{"issue":"11","key":"6575_CR52","doi-asserted-by":"publisher","first-page":"654","DOI":"10.1038\/s41574-020-0386-0","volume":"16","author":"L Geng","year":"2020","unstructured":"Geng L, Lam KSL, Xu A (2020) The therapeutic potential of FGF21 in metabolic diseases: from bench to clinic. Nat Rev Endocrinol 16(11):654\u2013667. https:\/\/doi.org\/10.1038\/s41574-020-0386-0","journal-title":"Nat Rev Endocrinol"},{"issue":"1","key":"6575_CR53","doi-asserted-by":"publisher","first-page":"1661","DOI":"10.1038\/s41467-025-56885-9","volume":"16","author":"K Zhang","year":"2025","unstructured":"Zhang K, Gan J, Wang B et al (2025) FGF21 protects against HFpEF by improving cardiac mitochondrial bioenergetics in mice. Nat Commun 16(1):1661. https:\/\/doi.org\/10.1038\/s41467-025-56885-9","journal-title":"Nat Commun"},{"issue":"9","key":"6575_CR54","doi-asserted-by":"publisher","first-page":"2470","DOI":"10.2337\/db05-1435","volume":"55","author":"W Wente","year":"2006","unstructured":"Wente W, Efanov AM, Brenner M et al (2006) Fibroblast growth factor-21 improves pancreatic \u03b2-cell function and survival by activation of extracellular signal-regulated kinase 1\/2 and Akt signaling pathways. Diabetes 55(9):2470\u20132478. https:\/\/doi.org\/10.2337\/db05-1435","journal-title":"Diabetes"},{"issue":"1","key":"6575_CR55","doi-asserted-by":"publisher","first-page":"19","DOI":"10.1093\/cvr\/cvu263","volume":"106","author":"A Planavila","year":"2015","unstructured":"Planavila A, Redondo-Angulo I, Ribas F et al (2015) Fibroblast growth factor 21 protects the heart from oxidative stress. Cardiovasc Res 106(1):19\u201331. https:\/\/doi.org\/10.1093\/cvr\/cvu263","journal-title":"Cardiovasc Res"},{"key":"6575_CR56","doi-asserted-by":"publisher","first-page":"335","DOI":"10.1016\/j.redox.2016.12.024","volume":"11","author":"MA Gomez-Samano","year":"2017","unstructured":"Gomez-Samano MA, Grajales-Gomez M, Zuarth-Vazquez JM et al (2017) Fibroblast growth factor 21 and its novel association with oxidative stress. Redox Biol 11:335\u2013341. https:\/\/doi.org\/10.1016\/j.redox.2016.12.024","journal-title":"Redox Biol"},{"issue":"22","key":"6575_CR57","doi-asserted-by":"publisher","first-page":"2290","DOI":"10.1212\/WNL.0000000000003374","volume":"87","author":"JM Lehtonen","year":"2016","unstructured":"Lehtonen JM, Forsstrom S, Bottani E et al (2016) FGF21 is a biomarker for mitochondrial translation and mtDNA maintenance disorders. Neurology 87(22):2290\u20132299. https:\/\/doi.org\/10.1212\/WNL.0000000000003374","journal-title":"Neurology"},{"issue":"1","key":"6575_CR58","doi-asserted-by":"publisher","first-page":"22","DOI":"10.1038\/s42003-022-04303-x","volume":"6","author":"G Sturm","year":"2023","unstructured":"Sturm G, Karan KR, Monzel AS et al (2023) OxPhos defects cause hypermetabolism and reduce lifespan in cells and in patients with mitochondrial diseases. Commun Biol 6(1):22. https:\/\/doi.org\/10.1038\/s42003-022-04303-x","journal-title":"Commun Biol"},{"issue":"9","key":"6575_CR59","doi-asserted-by":"publisher","first-page":"979","DOI":"10.1038\/s41374-022-00787-7","volume":"102","author":"B Li","year":"2022","unstructured":"Li B, Liu L (2022) Fibroblast growth factor 21, a stress regulator, inhibits Drp1 activation to alleviate skeletal muscle ischemia\/reperfusion injury. Lab Invest 102(9):979\u2013988. https:\/\/doi.org\/10.1038\/s41374-022-00787-7","journal-title":"Lab Invest"},{"issue":"3","key":"6575_CR60","doi-asserted-by":"publisher","first-page":"487","DOI":"10.1038\/s41418-018-0133-4","volume":"26","author":"J Knupp","year":"2019","unstructured":"Knupp J, Arvan P, Chang A (2019) Increased mitochondrial respiration promotes survival from endoplasmic reticulum stress. Cell Death Differ 26(3):487\u2013501. https:\/\/doi.org\/10.1038\/s41418-018-0133-4","journal-title":"Cell Death Differ"},{"key":"6575_CR61","doi-asserted-by":"publisher","first-page":"e41351","DOI":"10.7554\/eLife.41351","volume":"8","author":"CH Yao","year":"2019","unstructured":"Yao CH, Wang R, Wang Y, Kung CP, Weber JD, Patti GJ (2019) Mitochondrial fusion supports increased oxidative phosphorylation during cell proliferation. Elife 8:e41351. https:\/\/doi.org\/10.7554\/eLife.41351","journal-title":"Elife"},{"key":"6575_CR62","doi-asserted-by":"publisher","first-page":"101489","DOI":"10.1016\/j.molmet.2022.101489","volume":"60","author":"X Yu","year":"2022","unstructured":"Yu X, Arden C, Berlinguer-Palmini R et al (2022) Mitochondrial complex I subunit deficiency promotes pancreatic \u03b1-cell proliferation. Mol Metab 60:101489. https:\/\/doi.org\/10.1016\/j.molmet.2022.101489","journal-title":"Mol Metab"},{"issue":"1","key":"6575_CR63","doi-asserted-by":"publisher","first-page":"53","DOI":"10.1530\/JOE-19-0451","volume":"245","author":"N Tanday","year":"2020","unstructured":"Tanday N, Flatt PR, Irwin N, Moffett RC (2020) Liraglutide and sitagliptin counter beta- to alpha-cell transdifferentiation in diabetes. J Endocrinol 245(1):53\u201364. https:\/\/doi.org\/10.1530\/JOE-19-0451","journal-title":"J Endocrinol"},{"issue":"11","key":"6575_CR64","doi-asserted-by":"publisher","first-page":"3300","DOI":"10.1016\/j.celrep.2018.05.035","volume":"23","author":"LJB Briant","year":"2018","unstructured":"Briant LJB, Dodd MS, Chibalina MV et al (2018) CPT1a-dependent long-chain fatty acid oxidation contributes to maintaining glucagon secretion from pancreatic islets. Cell Rep 23(11):3300\u20133311. https:\/\/doi.org\/10.1016\/j.celrep.2018.05.035","journal-title":"Cell Rep"},{"key":"6575_CR65","doi-asserted-by":"publisher","first-page":"155915","DOI":"10.1016\/j.metabol.2024.155915","volume":"156","author":"MM Richter","year":"2024","unstructured":"Richter MM, Kemp IM, Heeboll S et al (2024) Glucagon augments the secretion of FGF21 and GDF15 in MASLD by indirect mechanisms. Metabolism 156:155915. https:\/\/doi.org\/10.1016\/j.metabol.2024.155915","journal-title":"Metabolism"},{"issue":"1","key":"6575_CR66","doi-asserted-by":"publisher","first-page":"148","DOI":"10.1186\/s12933-018-0791-z","volume":"17","author":"J Hernandez-Cascales","year":"2018","unstructured":"Hernandez-Cascales J (2018) Does glucagon have a positive inotropic effect in the human heart? Cardiovasc Diabetol 17(1):148. https:\/\/doi.org\/10.1186\/s12933-018-0791-z","journal-title":"Cardiovasc Diabetol"},{"issue":"5","key":"6575_CR67","doi-asserted-by":"publisher","first-page":"614","DOI":"10.1161\/CIRCRESAHA.124.324706","volume":"135","author":"C Gao","year":"2024","unstructured":"Gao C, Xiong Z, Liu Y et al (2024) Glucagon receptor antagonist for heart failure with preserved ejection fraction. Circ Res 135(5):614\u2013628. https:\/\/doi.org\/10.1161\/CIRCRESAHA.124.324706","journal-title":"Circ Res"},{"issue":"3","key":"6575_CR68","doi-asserted-by":"publisher","first-page":"549","DOI":"10.1016\/j.cmet.2018.01.015","volume":"27","author":"R Rodriguez-Diaz","year":"2018","unstructured":"Rodriguez-Diaz R, Molano RD, Weitz JR et al (2018) Paracrine interactions within the pancreatic islet determine the glycemic set point. Cell Metab 27(3):549-558 e544. https:\/\/doi.org\/10.1016\/j.cmet.2018.01.015","journal-title":"Cell Metab"},{"issue":"5","key":"6575_CR69","doi-asserted-by":"publisher","first-page":"599","DOI":"10.2337\/db22-0784","volume":"72","author":"T Wei","year":"2023","unstructured":"Wei T, Cui X, Jiang Y et al (2023) Glucagon acting at the GLP-1 receptor contributes to \u03b2-cell regeneration induced by glucagon receptor antagonism in diabetic mice. Diabetes 72(5):599\u2013610. https:\/\/doi.org\/10.2337\/db22-0784","journal-title":"Diabetes"},{"issue":"Pt 2","key":"6575_CR70","doi-asserted-by":"publisher","first-page":"287","DOI":"10.1042\/BJ20021288","volume":"369","author":"T Tsuboi","year":"2003","unstructured":"Tsuboi T, da Silva Xavier G, Holz GG, Jouaville LS, Thomas AP, Rutter GA (2003) Glucagon-like peptide-1 mobilizes intracellular Ca2+ and stimulates mitochondrial ATP synthesis in pancreatic MIN6 beta-cells. Biochem J 369(Pt 2):287\u2013299. https:\/\/doi.org\/10.1042\/BJ20021288","journal-title":"Biochem J"},{"issue":"11","key":"6575_CR71","doi-asserted-by":"publisher","first-page":"773","DOI":"10.1042\/BCJ20230167","volume":"480","author":"GA Rutter","year":"2023","unstructured":"Rutter GA, Sidarala V, Kaufman BA, Soleimanpour SA (2023) Mitochondrial metabolism and dynamics in pancreatic beta cell glucose sensing. Biochem J 480(11):773\u2013789. https:\/\/doi.org\/10.1042\/BCJ20230167","journal-title":"Biochem J"},{"issue":"7","key":"6575_CR72","doi-asserted-by":"publisher","first-page":"1472","DOI":"10.2337\/db21-0800","volume":"71","author":"E Georgiadou","year":"2022","unstructured":"Georgiadou E, Muralidharan C, Martinez M et al (2022) Mitofusins Mfn1 and Mfn2 are required to preserve glucose- but not incretin-stimulated \u03b2-cell connectivity and insulin secretion. Diabetes 71(7):1472\u20131489. https:\/\/doi.org\/10.2337\/db21-0800","journal-title":"Diabetes"},{"key":"6575_CR73","doi-asserted-by":"publisher","first-page":"90","DOI":"10.3389\/fcell.2017.00090","volume":"5","author":"J Dudek","year":"2017","unstructured":"Dudek J (2017) Role of cardiolipin in mitochondrial signaling pathways. Front Cell Dev Biol 5:90. https:\/\/doi.org\/10.3389\/fcell.2017.00090","journal-title":"Front Cell Dev Biol"},{"key":"6575_CR74","doi-asserted-by":"publisher","unstructured":"Wohlfarter Y, Hagenbuchner J, Horzum U et al (2024) Mitochondrial cardiolipin metabolism controlled by tafazzin enables ferroptosis. BioRxiv 2024.10.25.620299 (Preprint). 26 Oct 2024. Available from: https:\/\/doi.org\/10.1101\/2024.10.25.620299","DOI":"10.1101\/2024.10.25.620299"},{"issue":"1","key":"6575_CR75","doi-asserted-by":"publisher","first-page":"e202302335","DOI":"10.26508\/lsa.202302335","volume":"7","author":"A Janer","year":"2024","unstructured":"Janer A, Morris JL, Krols M et al (2024) ESYT1 tethers the ER to mitochondria and is required for mitochondrial lipid and calcium homeostasis. Life Sci Alliance 7(1):e202302335. https:\/\/doi.org\/10.26508\/lsa.202302335","journal-title":"Life Sci Alliance"},{"issue":"1","key":"6575_CR76","doi-asserted-by":"publisher","first-page":"7","DOI":"10.1111\/jnc.14242","volume":"144","author":"I Akan","year":"2018","unstructured":"Akan I, Olivier-Van Stichelen S, Bond MR, Hanover JA (2018) Nutrient-driven O-GlcNAc in proteostasis and neurodegeneration. J Neurochem 144(1):7\u201334. https:\/\/doi.org\/10.1111\/jnc.14242","journal-title":"J Neurochem"},{"issue":"5","key":"6575_CR77","doi-asserted-by":"publisher","first-page":"107609","DOI":"10.1016\/j.celrep.2020.107609","volume":"31","author":"A Lockridge","year":"2020","unstructured":"Lockridge A, Jo S, Gustafson E et al (2020) Islet O-GlcNAcylation is required for lipid potentiation of insulin secretion through SERCA2. Cell Rep 31(5):107609. https:\/\/doi.org\/10.1016\/j.celrep.2020.107609","journal-title":"Cell Rep"},{"issue":"11","key":"6575_CR78","doi-asserted-by":"publisher","first-page":"648","DOI":"10.1016\/j.lfs.2012.06.011","volume":"92","author":"SA Marsh","year":"2013","unstructured":"Marsh SA, Powell PC, Dell\u2019italia LJ, Chatham JC (2013) Cardiac O-GlcNAcylation blunts autophagic signaling in the diabetic heart. Life Sci 92(11):648\u2013656. https:\/\/doi.org\/10.1016\/j.lfs.2012.06.011","journal-title":"Life Sci"},{"issue":"36","key":"6575_CR79","doi-asserted-by":"publisher","first-page":"14940","DOI":"10.1074\/jbc.M117.797944","volume":"292","author":"EP Tan","year":"2017","unstructured":"Tan EP, McGreal SR, Graw S et al (2017) Sustained O-GlcNAcylation reprograms mitochondrial function to regulate energy metabolism. J Biol Chem 292(36):14940\u201314962. https:\/\/doi.org\/10.1074\/jbc.M117.797944","journal-title":"J Biol Chem"},{"issue":"5","key":"6575_CR80","doi-asserted-by":"publisher","first-page":"2107","DOI":"10.1074\/jbc.M115.693580","volume":"291","author":"SP Durning","year":"2016","unstructured":"Durning SP, Flanagan-Steet H, Prasad N, Wells L (2016) O-Linked \u03b2-N-acetylglucosamine (O-GlcNAc) acts as a glucose sensor to epigenetically regulate the insulin gene in pancreatic beta cells. J Biol Chem 291(5):2107\u20132118. https:\/\/doi.org\/10.1074\/jbc.M115.693580","journal-title":"J Biol Chem"}],"container-title":["Diabetologia"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/link.springer.com\/content\/pdf\/10.1007\/s00125-025-06575-4.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/link.springer.com\/article\/10.1007\/s00125-025-06575-4\/fulltext.html","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/link.springer.com\/content\/pdf\/10.1007\/s00125-025-06575-4.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,12,8]],"date-time":"2025-12-08T09:14:29Z","timestamp":1765185269000},"score":1,"resource":{"primary":{"URL":"https:\/\/link.springer.com\/10.1007\/s00125-025-06575-4"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2025,10,24]]},"references-count":80,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2026,1]]}},"alternative-id":["6575"],"URL":"https:\/\/doi.org\/10.1007\/s00125-025-06575-4","relation":{},"ISSN":["0012-186X","1432-0428"],"issn-type":[{"value":"0012-186X","type":"print"},{"value":"1432-0428","type":"electronic"}],"subject":[],"published":{"date-parts":[[2025,10,24]]},"assertion":[{"value":"16 October 2024","order":1,"name":"received","label":"Received","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"25 July 2025","order":2,"name":"accepted","label":"Accepted","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"24 October 2025","order":3,"name":"first_online","label":"First Online","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"We thank A. Schniebs, A. Armbr\u00fcster, S. Janku (Department of Biophysics, Saarland University) and R. Nickels (Institute for Clinical and Experimental Surgery, Saarland University) for excellent technical assistance. We also thank G. Stopper (Department of Biophysics, Saarland University) for software and data analysis support.","order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Acknowledgements"}},{"value":"The complete gene list of RNA-seq data and lipidomics profile information (including lipid class, species, double bond, hydroxylation, carbon length and fatty acid profiles) are in online deposit:\n                      \n                      . All other data will be made available upon request.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Data availability"}},{"value":"Open Access funding enabled and organized by Projekt DEAL. BM is grateful for generous support from the German Research Foundation (DFG), MO 2774\/7-1 project number 508372800 and MO 2774\/6-1 project number 505680640. CC was partially supported by the DFG SFB894. LPR is grateful for support from DFG TRR 219 Project ID 322900939. CM was and is supported by the Deutsche Forschungsgemeinschaft (DFG; SFB 894, Project A13; and SFB 1525, project # 453989101; Ma 2528\/7-1; 8-1, project #505805397; and 9-2, project #315254108).","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Funding"}},{"value":"CM has received speaker honoraria and has served as an advisor to AstraZeneca, Bristol Myers Squibb, Boehringer Ingelheim, Cytokinestics, Lilly and Novo Nordisk. The other authors declare that there are no relationships or activities that might bias, or be perceived to bias, their work.","order":4,"name":"Ethics","group":{"name":"EthicsHeading","label":"Authors\u2019 relationships and activities"}},{"value":"CC, MDAH, CB, AGA, AL, L-AdS, JA-C, SW, EB, TH, KvdM and LPR performed the experiments and analysed the data. CC, MAL, MB, MH, PG, MAR, MvdL, BM, EA, JD, EB and CM discussed the data, analysed and interpreted the data, and provided materials and equipment. CM and LPR acquired funding and designed the project. CC and LPR designed the experiments, supervised the project and wrote the paper. All authors read and approved the manuscript to be published. All authors listed in this manuscript fulfil the following criteria: (1) substantial contributions to the conception or design of the work; or the acquisition, analysis or interpretation of data; (2) drafting the article or reviewing it critically for important intellectual content; and (3) final approval of the version to be published. LPR is responsible for the integrity of the work as a whole.","order":5,"name":"Ethics","group":{"name":"EthicsHeading","label":"Contribution statement"}}]}}