{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T19:32:37Z","timestamp":1792006357973,"version":"4.4.0"},"reference-count":48,"publisher":"American Diabetes Association","issue":"2","license":[{"start":{"date-parts":[[2025,12,1]],"date-time":"2025-12-01T00:00:00Z","timestamp":1764547200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.diabetesjournals.org\/journals\/pages\/license"}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,2,1]]},"abstract":"<jats:sec>\n                    <jats:title\/>\n                    <jats:p>Pancreatic fibrosis has been proposed as a contributor to type 2 diabetes (T2D) by impairing islet function, but whether it plays a causal role remains unclear. We investigated this question using two complementary approaches. First, we performed a computed tomography\u2013based retrospective case-control study (T2D case patients: n = 58; control participants: n = 58) assessing extracellular volume fraction as a marker of fibrosis in the pancreas, liver, and myocardium. Greater pancreatic fibrosis was associated with T2D (adjusted odds ratio [OR] per 1 [SD] increase: 1.64; 95% CI 1.00\u20132.68), independent of age, sex, BMI, liver fibrosis, and myocardial fibrosis. Second, we conducted a Mendelian randomization analysis using genome-wide association study (GWAS) data on multiorgan fibrosis derived from MRI in the UK Biobank (n = 43,881), along with T2D GWAS data from the Diabetes Genetics Replication and Meta-analysis (DIAGRAM) consortium (n = 242,283 T2D case patients and 1,569,734 control participants). Genetically predicted pancreatic fibrosis levels were associated with an increased T2D risk (OR per 1-SD increase: 1.43; 95% CI 1.09\u20131.89), whereas liver and myocardial fibrosis levels showed no associations. These findings support a potential causal and organ-specific role of pancreatic fibrosis in the pathogenesis of T2D, highlighting pancreatic fibrosis as a mechanistically plausible and potentially targetable target in diabetes prevention.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Article Highlights<\/jats:title>\n                    <jats:p>Pancreatic, but not liver or myocardial, fibrosis is specifically and independently linked to type 2 diabetes. Mendelian randomization analysis reveals a causal role of pancreatic fibrosis in diabetes development. Pancreatic fibrosis might be a potential therapeutic target to preserve \u03b2-cell function and prevent diabetes.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2337\/db25-0629","type":"journal-article","created":{"date-parts":[[2025,12,1]],"date-time":"2025-12-01T15:02:48Z","timestamp":1764601368000},"page":"369-378","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":6,"title":["Multiorgan Fibrosis and Risk of Type 2 Diabetes: Genetic and Observational Evidence Highlighting a Causal Role of Pancreatic Fibrosis"],"prefix":"10.2337","volume":"75","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-3870-6543","authenticated-orcid":false,"given":"Masato","family":"Uchida","sequence":"first","affiliation":[{"name":"Department of General Internal Medicine, Hashimoto Municipal Hospital 1 , Wakayama, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9034-4370","authenticated-orcid":false,"given":"Hajime","family":"Yamazaki","sequence":"additional","affiliation":[{"name":"Department of Community Medicine, Section of Clinical Epidemiology, Graduate School of Medicine, Kyoto University 2 , Kyoto, Japan"},{"name":"Center for Innovative Research for Communities and Clinical Excellence, Fukushima Medical University 3 , Fukushima, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sihao","family":"Han","sequence":"additional","affiliation":[{"name":"Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California 4 , Los Angeles, CA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian Z.","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California 4 , Los Angeles, CA"},{"name":"Norris Comprehensive Cancer Center, University of Southern California 5 , Los Angeles, CA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shoko","family":"Ariyoshi","sequence":"additional","affiliation":[{"name":"Department of General Internal Medicine, Hashimoto Municipal Hospital 1 , Wakayama, Japan"},{"name":"Department of General Internal Medicine, Japan Community Healthcare Organization Kyushu Hospital 6 , Fukuoka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoji","family":"Hirayama","sequence":"additional","affiliation":[{"name":"Department of General Internal Medicine, Hashimoto Municipal Hospital 1 , Wakayama, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sho","family":"Matsushita","sequence":"additional","affiliation":[{"name":"Department of General Internal Medicine, Hashimoto Municipal Hospital 1 , Wakayama, 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