{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T16:24:45Z","timestamp":1789230285726,"version":"build-2803163510"},"reference-count":31,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2019,7,27]],"date-time":"2019-07-27T00:00:00Z","timestamp":1564185600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Diabetes Invest"],"published-print":{"date-parts":[[2020,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Aims\/Introduction<\/jats:title><jats:p>The relationship between pancreatic fatty infiltration and diabetes is widely known, whereas the causal relationship is not clear. Furthermore, it is uncertain whether pathogenesis of pancreatic fat is similar to that of liver fat. We aimed to clarify the contribution of this type of fat to glucose metabolism in type\u00a02 diabetes patients by cross\u2010sectional and longitudinal analyses.<\/jats:p><\/jats:sec><jats:sec><jats:title>Material and Methods<\/jats:title><jats:p>A total of 56 patients with type\u00a02 diabetes who had been hospitalized twice were analyzed. We evaluated the mean computed tomography values of the pancreas (P), liver (L) and spleen (S). Lower <jats:styled-content style=\"fixed-case\">computed tomography<\/jats:styled-content> values indicate a greater fat content. We defined indices of pancreatic or liver fat content as the differences between P or L and S. We assessed the associations among fat content for the two organs (P\u2010S, L\u2010S) and clinical parameters at the first hospitalization, and then analyzed the associations between these fat contents and changes in glycometabolic markers (the second data values minus the first).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In the cross\u2010sectional study, P\u2010S negatively correlated with the increment of C\u2010peptide in the glucagon stimulation test (<jats:italic>r<\/jats:italic>\u00a0=\u00a0\u22120.71, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.0001) and body mass index (<jats:italic>r<\/jats:italic>\u00a0=\u00a0\u22120.28, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.034). L\u2010S negatively correlated with homeostasis model assessment of insulin resistance (<jats:italic>r<\/jats:italic>\u00a0=\u00a0\u22120.73, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.0001), <jats:styled-content style=\"fixed-case\">body mass index<\/jats:styled-content> (<jats:italic>r<\/jats:italic>\u00a0=\u00a0\u22120.62, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.0001) and some other obesity\u2010related indicators, but not with the increment of C\u2010peptide in the glucagon stimulation test. In the longitudinal study, P\u2010S positively correlated with the change of the increment of C\u2010peptide in the glucagon stimulation test (<jats:italic>r<\/jats:italic>\u00a0=\u00a00.49, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.021).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>In type\u00a02 diabetes patients, pancreatic fat was less associated with obesity\u2010related indicators than liver fat, but was more strongly associated with the longitudinal decrease in endogenous insulin\u2010secreting capacity.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jdi.13108","type":"journal-article","created":{"date-parts":[[2019,6,26]],"date-time":"2019-06-26T06:53:07Z","timestamp":1561531987000},"page":"80-87","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["Pancreatic fat is related to the longitudinal decrease in the increment of C\u2010peptide in glucagon stimulation test in type\u00a02 diabetes patients"],"prefix":"10.1111","volume":"11","author":[{"given":"Chisaki","family":"Ishibashi","sequence":"first","affiliation":[{"name":"Department of Metabolic Medicine Graduate School of Medicine Osaka University Suita Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9665-8947","authenticated-orcid":false,"given":"Junji","family":"Kozawa","sequence":"additional","affiliation":[{"name":"Department of Metabolic Medicine Graduate School of Medicine Osaka University Suita Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5505-1724","authenticated-orcid":false,"given":"Yoshiya","family":"Hosakawa","sequence":"additional","affiliation":[{"name":"Department of Metabolic Medicine Graduate School of Medicine Osaka University Suita Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sho","family":"Yoneda","sequence":"additional","affiliation":[{"name":"Department 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