{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T18:50:28Z","timestamp":1785351028080,"version":"3.55.0"},"reference-count":28,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T00:00:00Z","timestamp":1773014400000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,3,1]],"date-time":"2026-03-01T00:00:00Z","timestamp":1772323200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100006407","name":"Natural Science Foundation of Henan Province","doi-asserted-by":"publisher","award":["2023J05272"],"award-info":[{"award-number":["2023J05272"]}],"id":[{"id":"10.13039\/501100006407","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81770637"],"award-info":[{"award-number":["81770637"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82070667"],"award-info":[{"award-number":["82070667"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunity Inflam &amp;amp; Disease"],"published-print":{"date-parts":[[2026,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Adipose tissue (AT) playing a crucial role in obesity\u2010related pancreatitis. This study investigated the impact of autophagy in AT on pancreatic injury during obesity\u2010related severe acute pancreatitis (SAP).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Non\u2010obese and obese mice were induced using a normal diet (ND) or high\u2010fat diet (HFD) before establishing SAP. Pancreatic injury and autophagy in AT were evaluated. Adipose tissue macrophages (ATMs) were analyzed. Autophagy in RAW 264.7 cells co\u2010cultured with palmitic acid (PA) and lipopolysaccharide (LPS), simulating the conditions of ATMs during SAP, was further investigated. The effect of PA on autophagy within inflammatory macrophages in vitro was explored, utilizing Sulfo\u2010N\u2010succinimidyloleate (SSO) to inhibit fatty acid transport. Additionally, the impact of autophagy in AT on inflammation in SAP mice was investigated using SSO, complemented by metabolomics analysis to uncover underlying molecular mechanisms.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Pancreatic histological scores were significantly higher in obese SAP mice than in non\u2011obese SAP mice (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u20096; 9.50\u2009\u00b1\u20091.05 vs. 7.33\u2009\u00b1\u20091.03;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.0005). Impaired autophagic flux was observed in the AT of obese SAP mice compared with obese control mice, as indicated by increased LC3\u2011II (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.0383) and p62 levels (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.0171). PA induced impaired autophagic flux in inflammatory macrophages. Inhibition of fatty acid transport partially restored impaired autophagic flux in an ATM cell model of SAP. Furthermore, this inhibition also alleviated the impairment of autophagic flux in AT and attenuated pancreatic injury in obese SAP mice. Metabolomics analysis of AT revealed elevated levels of more fatty acids and several signaling pathways correlated with autophagy in obese SAP mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Impaired autophagic flux in AT aggravates pancreatic injury in obese SAP mice, with impaired autophagic flux in ATMs likely playing a crucial role. Metabolomics analysis revealed abnormal lipid metabolism in AT of obese SAP mice, and several signaling pathways may contribute to impaired autophagic flux in this tissue.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/iid3.70395","type":"journal-article","created":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T16:06:17Z","timestamp":1773072377000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Impaired Autophagic Flux in Adipose Tissue Aggravates Pancreatic Injury in Obesity\u2010Related Severe Acute Pancreatitis"],"prefix":"10.1002","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6490-3845","authenticated-orcid":false,"given":"Li\u2010Ping","family":"Sheng","sequence":"first","affiliation":[{"name":"Department of Gastroenterology, the First Affiliated Hospital of Xiamen University, School of Medicine Xiamen University Xiamen China"},{"name":"Department of Gastroenterology, Union Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guo\u2010Chen","family":"Shang","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, Union Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan China"},{"name":"Department of Gastroenterology, the First Affiliated Hospital, School of Medicine Shihezi University Shihezi China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chao\u2010Qun","family":"Han","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, Union Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin","family":"Ling","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, Union Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan China"},{"name":"Department of Gastroenterology, the First Affiliated Hospital Sun Yat\u2010sen University Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xian\u2010Wen","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, Union Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rong","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, Union Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhen","family":"Ding","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, Union Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan China"},{"name":"Department of Gastroenterology, the First 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