{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,1]],"date-time":"2026-06-01T22:45:25Z","timestamp":1780353925058,"version":"3.54.1"},"reference-count":43,"publisher":"American Diabetes Association","issue":"11","license":[{"start":{"date-parts":[[2024,8,13]],"date-time":"2024-08-13T00:00:00Z","timestamp":1723507200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.diabetesjournals.org\/journals\/pages\/license"}],"funder":[{"name":"Soci\u00e9t\u00e9rancophone du Diab\u00e8te"},{"name":"National Center for Precision Diabetic Medicine"},{"name":"Horizon Europe Research and Innovation Programme","award":["101080465"],"award-info":[{"award-number":["101080465"]}]},{"name":"Horizon Europe Research and Innovation Programme","award":["ANR-10-INBS-009"],"award-info":[{"award-number":["ANR-10-INBS-009"]}]},{"name":"European Genomics Institute for Diabetes","award":["ANR-10-EQPX-07-01"],"award-info":[{"award-number":["ANR-10-EQPX-07-01"]}]},{"name":"Lille Integrated Genomics Advanced Network"},{"name":"Agence Nationale de la Recherche [ANR]"},{"DOI":"10.13039\/501100000781","name":"European Research Council","doi-asserted-by":"publisher","award":["101043671"],"award-info":[{"award-number":["101043671"]}],"id":[{"id":"10.13039\/501100000781","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2024,11,1]]},"abstract":"<jats:sec>\n                  <jats:title\/>\n                  <jats:p>We postulated that type 2 diabetes (T2D) predisposes patients to exocrine pancreatic diseases through (epi)genetic mechanisms. We explored the methylome (using MethylationEPIC arrays) of the exocrine pancreas in 141 donors, assessing the impact of T2D. An epigenome-wide association study of T2D identified hypermethylation in an enhancer of the pancreatic lipase\u2013related protein 1 (PNLIPRP1) gene, associated with decreased PNLIPRP1 expression. PNLIPRP1 null variants (found in 191,000 participants in the UK Biobank) were associated with elevated glycemia and LDL cholesterol. Mendelian randomization using 2.5M SNP Omni arrays in 111 donors revealed that T2D was causal of PNLIPRP1 hypermethylation, which in turn was causal of LDL cholesterol. Additional AR42J rat exocrine cell analyses demonstrated that Pnliprp1 knockdown induced acinar-to-ductal metaplasia, a known prepancreatic cancer state, and increased cholesterol levels, reversible with statin. This (epi)genetic study suggests a role for PNLIPRP1 in human metabolism and exocrine pancreatic function, with potential implications for pancreatic diseases.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Article Highlights<\/jats:title>\n               <\/jats:sec>","DOI":"10.2337\/db24-0215","type":"journal-article","created":{"date-parts":[[2024,8,13]],"date-time":"2024-08-13T16:31:05Z","timestamp":1723566665000},"page":"1908-1918","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":4,"title":["<i>PNLIPRP1<\/i> Hypermethylation in Exocrine Pancreas Links Type 2 Diabetes and Cholesterol Metabolism"],"prefix":"10.2337","volume":"73","author":[{"given":"Lucas","family":"Maurin","sequence":"first","affiliation":[{"name":"1INSERM UMR 1283, CNRS UMR 8199, European Genomic Institute for Diabetes, Institut Pasteur de Lille, Lille, France"},{"name":"2Lille University Hospital, 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