{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T14:28:42Z","timestamp":1785767322534,"version":"3.56.0"},"reference-count":58,"publisher":"American Diabetes Association","issue":"11","license":[{"start":{"date-parts":[[2025,9,4]],"date-time":"2025-09-04T00:00:00Z","timestamp":1756944000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.diabetesjournals.org\/journals\/pages\/license"}],"funder":[{"name":"Breakthrough Type 1 Diabetes","award":["SRA-2024-1553"],"award-info":[{"award-number":["SRA-2024-1553"]}]},{"DOI":"10.13039\/100000005","name":"US Department of Defense","doi-asserted-by":"crossref","award":["W81XWH-20-1-200"],"award-info":[{"award-number":["W81XWH-20-1-200"]}],"id":[{"id":"10.13039\/100000005","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["F31 DK139619"],"award-info":[{"award-number":["F31 DK139619"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 DK140093"],"award-info":[{"award-number":["R01 DK140093"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Fraternal Order of Eagles Diabetes Research Center, University of Iowa","award":["Pilot and Feasibility award"],"award-info":[{"award-number":["Pilot and Feasibility award"]}]}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,11,1]]},"abstract":"<jats:sec>\n                    <jats:title\/>\n                    <jats:p>Type 1 diabetes (T1D) is caused by the selective autoimmune ablation of pancreatic \u03b2-cells. Emerging evidence reveals \u03b2-cell secretory dysfunction arises early in T1D development and may contribute to diseases etiology; however, the underlying mechanisms are not well understood. Our data reveal that proinflammatory cytokines elicit a complex change in the \u03b2-cell\u2019s Golgi structure and function. The structural modifications include Golgi compaction and loss of the interconnecting ribbon resulting in Golgi fragmentation. We further show that Golgi structural alterations coincide with persistent altered cell surface glycoprotein composition. Our data demonstrate that inducible nitric oxide synthase (iNOS)\u2013generated nitric oxide (NO) is necessary and sufficient for \u03b2-cell Golgi restructuring. Moreover, the unique sensitivity of the \u03b2-cell to NO-dependent mitochondrial inhibition results in \u03b2-cell\u2013specific Golgi alterations that are absent in other cell types, including \u03b1-cells. Examination of human pancreas samples from autoantibody-positive and T1D donors with residual \u03b2-cells further revealed alterations in \u03b2-cell, but not \u03b1-cell, Golgi structure that correlate with T1D progression. Collectively, our studies provide critical clues as to how \u03b2-cell secretory functions are specifically impacted by cytokines and NO that may contribute to the development of \u03b2-cell autoantigens relevant to T1D.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Article Highlights<\/jats:title>\n                    <jats:p>Proinflammatory cytokines drive disruptions in Golgi structure and function in human, mouse, and rat \u03b2-cells. Golgi alterations result from inducible nitric oxide synthase (iNOS)\u2013 and nitric oxide (NO)\u2013dependent inhibition of mitochondrial metabolism. \u03b1-Cell Golgi structure is insensitive to cytokine- and NO-mediated metabolic inhibition. Analysis of human donor tissue shows early Golgi alteration in \u03b2-cells from autoantibody-positive donors, which persists in residual \u03b2-cells from T1D donors.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2337\/db25-0132","type":"journal-article","created":{"date-parts":[[2025,9,4]],"date-time":"2025-09-04T16:07:40Z","timestamp":1757002060000},"page":"1992-2007","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":5,"title":["Proinflammatory Cytokines Mediate Pancreatic \u03b2-Cell\u2013Specific Alterations to Golgi Integrity via iNOS-Dependent Mitochondrial Inhibition"],"prefix":"10.2337","volume":"74","author":[{"given":"Sandra E.","family":"Blom","sequence":"first","affiliation":[{"name":"Fraternal Order of Eagles Diabetes Research Center, University of Iowa 1 , Iowa City, IA"},{"name":"Department of Internal Medicine, Division of Endocrinology and Metabolism, University of Iowa 2 , Iowa City, IA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Palin R.","family":"Narsian","sequence":"additional","affiliation":[{"name":"Fraternal Order of Eagles Diabetes Research Center, University of Iowa 1 , Iowa City, IA"},{"name":"Department of Internal Medicine, Division of Endocrinology and Metabolism, University of Iowa 2 , Iowa City, IA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Riley M.","family":"Behan-Bush","sequence":"additional","affiliation":[{"name":"Fraternal Order of Eagles Diabetes Research Center, University of Iowa 1 , Iowa City, IA"},{"name":"Roy J. Carver Department of Biomedical Engineering, University of Iowa 3 , Iowa City, IA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James A.","family":"Ankrum","sequence":"additional","affiliation":[{"name":"Fraternal Order of Eagles Diabetes Research Center, University of Iowa 1 , Iowa City, IA"},{"name":"Roy J. Carver Department of Biomedical Engineering, University of Iowa 3 , Iowa City, IA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ling","family":"Yang","sequence":"additional","affiliation":[{"name":"Fraternal Order of Eagles Diabetes Research Center, University of Iowa 1 , Iowa City, IA"},{"name":"Department of Anatomy and Cell Biology, University of Iowa 4 , Iowa City, IA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1152-2691","authenticated-orcid":false,"given":"Samuel B.","family":"Stephens","sequence":"additional","affiliation":[{"name":"Fraternal Order of Eagles Diabetes Research Center, University of Iowa 1 , Iowa City, IA"},{"name":"Department of Internal Medicine, Division of Endocrinology and Metabolism, University of Iowa 2 , Iowa City, IA"},{"name":"Department of Anatomy and Cell Biology, University of Iowa 4 , Iowa City, IA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1167","published-online":{"date-parts":[[2025,9,4]]},"reference":[{"key":"2026061115081209100_B1","doi-asserted-by":"crossref","first-page":"2449","DOI":"10.1016\/S0140-6736(18)31320-5","article-title":"Type 1 diabetes","volume":"391","author":"DiMeglio","year":"2018","journal-title":"Lancet"},{"key":"2026061115081209100_B2","doi-asserted-by":"crossref","first-page":"e120877","DOI":"10.1172\/jci.insight.120877","article-title":"\u03b2 Cell dysfunction exists more than 5 years before type 1 diabetes diagnosis","volume":"3","author":"Evans-Molina","year":"2018","journal-title":"JCI Insight"},{"key":"2026061115081209100_B3","doi-asserted-by":"crossref","first-page":"299","DOI":"10.1016\/B978-0-12-800174-5.00012-0","article-title":"\u03b2-Cell responses to nitric oxide","volume":"95","author":"Broniowska","year":"2014","journal-title":"Vitam Horm"},{"key":"2026061115081209100_B4","doi-asserted-by":"crossref","first-page":"21351","DOI":"10.1016\/S0021-9258(18)54642-1","article-title":"Interleukin-1 beta-induced formation of EPR-detectable iron-nitrosyl complexes in islets of Langerhans. 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