{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T16:53:06Z","timestamp":1791910386128,"version":"4.3.4"},"reference-count":50,"publisher":"American Diabetes Association","issue":"7","license":[{"start":{"date-parts":[[2025,4,9]],"date-time":"2025-04-09T00:00:00Z","timestamp":1744156800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.diabetesjournals.org\/journals\/pages\/license"}],"funder":[{"DOI":"10.13039\/501100021856","name":"Ministero dell'Universit\u00e0 e della Ricerca","doi-asserted-by":"publisher","award":["PNRR-MR1-2022-12375914"],"award-info":[{"award-number":["PNRR-MR1-2022-12375914"]}],"id":[{"id":"10.13039\/501100021856","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Private Donation"}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,7,1]]},"abstract":"<jats:sec>\n                    <jats:title\/>\n                    <jats:p>Wolfram syndrome 1 (WS1) is a rare genetic disorder caused by WFS1 variants that disrupt wolframin, an endoplasmic reticulum-associated protein essential for cellular stress responses, Ca2+ homeostasis, and autophagy. Here, we investigated how the c.316-1G&amp;gt;A and c.757A&amp;gt;T WFS1 mutations, which yield partially functional wolframin, affect the molecular functions of \u03b2-cells and explored the therapeutic potential of the glucagon-like peptide 1 receptor (GLP-1R) agonist liraglutide. Pancreatic \u03b2-cells obtained from patient-derived induced pluripotent stem cells (iPSCs) carrying this WFS1 variant exhibited reduced insulin processing and impaired secretory granule maturation, as evidenced by proinsulin accumulation and decreased prohormone convertase PC1\/3. Moreover, they exhibited dysregulated Ca2+ fluxes due to altered transcription of Ca2+-related genes, including CACNA1D, and significantly reduced SNAP25 levels, leading to uncoordinated oscillations and poor glucose responsiveness. Affected cells also showed increased autophagic flux and heightened susceptibility to inflammatory cytokine-induced apoptosis. Notably, liraglutide treatment rescued these defects by normalizing Ca2+ handling, enhancing insulin processing and secretion, and reducing apoptosis, likely through modulation of the unfolded protein response. These findings underscore the importance of defining mutation-specific dysfunctions in WS1 and support targeting the GLP-1\/GLP-1R axis as a therapeutic strategy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Article Highlights<\/jats:title>\n                    <jats:p>The molecular basis of WFS1-related mutations remains poorly investigated, and no definitive therapies exist for Wolfram syndrome 1. We dissected the molecular defects associated with c.316-1G&amp;gt;A and c.757A&amp;gt;T WFS1 mutations in patient-derived induced pluripotent stem cell islets and analyzed whether they are potential therapeutic targets of the glucagon-like peptide 1 receptor agonist liraglutide. We found impaired insulin granule maturation, altered Ca2+ fluxes, increased autophagic activity, and heightened susceptibility to inflammatory apoptosis in mutated cells. Liraglutide restored critical \u03b2-cell functions suggesting a route for personalized therapy based on WFS1 mutations.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2337\/db24-0720","type":"journal-article","created":{"date-parts":[[2025,4,9]],"date-time":"2025-04-09T10:50:41Z","timestamp":1744195841000},"page":"1273-1288","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":5,"title":["Liraglutide Treatment Reverses Unconventional Cellular Defects in Induced Pluripotent Stem Cell\u2013Derived \u03b2-Cells Harboring a Partially Functional\n                    <i>WFS1<\/i>\n                    Variant"],"prefix":"10.2337","volume":"74","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9908-2904","authenticated-orcid":false,"given":"Silvia","family":"Torchio","sequence":"first","affiliation":[{"name":"Unit of \u03b2 Cell Biology, Diabetes Research Institute, IRCCS San Raffaele Hospital 1 , Milan, Italy"},{"name":"Vita-Salute San Raffaele University 2 , Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7125-1745","authenticated-orcid":false,"given":"Gabriel","family":"Siracusano","sequence":"additional","affiliation":[{"name":"Unit of \u03b2 Cell Biology, Diabetes Research Institute, IRCCS San Raffaele Hospital 1 , Milan, Italy"},{"name":"Vita-Salute San Raffaele University 2 , Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8399-1281","authenticated-orcid":false,"given":"Federica","family":"Cuozzo","sequence":"additional","affiliation":[{"name":"Unit of \u03b2 Cell Biology, Diabetes Research Institute, IRCCS San Raffaele Hospital 1 , Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Valentina","family":"Zamarian","sequence":"additional","affiliation":[{"name":"Unit of \u03b2 Cell Biology, Diabetes Research Institute, IRCCS San Raffaele Hospital 1 , Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Silvia","family":"Pellegrini","sequence":"additional","affiliation":[{"name":"Unit of \u03b2 Cell Biology, Diabetes Research Institute, IRCCS San Raffaele Hospital 1 , Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabio","family":"Manenti","sequence":"additional","affiliation":[{"name":"Unit of \u03b2 Cell Biology, Diabetes Research Institute, IRCCS San Raffaele Hospital 1 , Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Riccardo","family":"Bonfanti","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, IRCCS San Raffaele Hospital 3 , Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6115-2476","authenticated-orcid":false,"given":"Giulio","family":"Frontino","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, IRCCS San Raffaele Hospital 3 , Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Valeria","family":"Sordi","sequence":"additional","affiliation":[{"name":"Unit of \u03b2 Cell Biology, Diabetes Research Institute, IRCCS San Raffaele Hospital 1 , Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4160-5386","authenticated-orcid":false,"given":"Raniero","family":"Chimienti","sequence":"additional","affiliation":[{"name":"Unit of \u03b2 Cell Biology, Diabetes Research Institute, IRCCS San Raffaele Hospital 1 , Milan, Italy"},{"name":"Vita-Salute San Raffaele University 2 , Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2172-2198","authenticated-orcid":false,"given":"Lorenzo","family":"Piemonti","sequence":"additional","affiliation":[{"name":"Unit of \u03b2 Cell Biology, Diabetes Research Institute, IRCCS San Raffaele Hospital 1 , Milan, Italy"},{"name":"Vita-Salute San Raffaele University 2 , Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1167","published-online":{"date-parts":[[2025,4,9]]},"reference":[{"key":"2026061113043084500_B1","doi-asserted-by":"crossref","first-page":"921","DOI":"10.1038\/pr.2018.17","article-title":"Genetic and clinical aspects of Wolfram syndrome 1, a severe neurodegenerative disease","volume":"83","author":"Rigoli","year":"2018","journal-title":"Pediatr Res"},{"key":"2026061113043084500_B2","doi-asserted-by":"crossref","first-page":"744","DOI":"10.1172\/JCI39678","article-title":"Wolfram syndrome 1 gene negatively regulates ER stress signaling in rodent and human cells","volume":"120","author":"Fonseca","year":"2010","journal-title":"J Clin Invest"},{"key":"2026061113043084500_B3","doi-asserted-by":"crossref","first-page":"5635","DOI":"10.1016\/j.febslet.2006.09.007","article-title":"WFS1 protein modulates the free Ca(2+) concentration in the endoplasmic 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