{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,4]],"date-time":"2026-06-04T14:27:57Z","timestamp":1780583277236,"version":"3.54.1"},"reference-count":23,"publisher":"The Endocrine Society","issue":"1","license":[{"start":{"date-parts":[[2021,9,2]],"date-time":"2021-09-02T00:00:00Z","timestamp":1630540800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["U34DK091958"],"award-info":[{"award-number":["U34DK091958"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000041","name":"American Diabetes Association","doi-asserted-by":"publisher","award":["1-14-D2d- 01"],"award-info":[{"award-number":["1-14-D2d- 01"]}],"id":[{"id":"10.13039\/100000041","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Context<\/jats:title>\n                  <jats:p>Vitamin D regulates glucose homeostasis pathways, but effects of vitamin D supplementation on \u03b2-cell function remain unclear.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Objective<\/jats:title>\n                  <jats:p>To investigate the effects of vitamin D3 supplementation on insulin sensitivity and \u03b2-cell function.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>This is a prespecified secondary analysis of the Vitamin D and Type 2 Diabetes study. Overweight\/obese adults at high risk for type 2 diabetes (prediabetes) were randomly treated with vitamin D3 4000 IU or matching placebo daily for 24 months.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Main Outcome<\/jats:title>\n                  <jats:p>Disposition index (DI), as an estimate of \u03b2-cell function, was calculated as the product of Homeostasis Model Assessment 2 indices derived from C-peptide values (HOMA2%Scpep) and C-peptide response during the first 30 minutes of a 75-g oral glucose tolerance test (OGTT).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>Mean age was 60.5 \u00b1 9.8 years and body mass index was 31.9 \u00b1 4.4 kg\/m2. Mean serum 25(OH)D level increased from 27.9 \u00b1 10.3 ng\/mL at baseline to 54.9 ng\/mL at 2 years in the vitamin D group and was unchanged (28.5 \u00b1 10.0 ng\/mL) in the placebo group. The baseline DI predicted incident diabetes independent of the intervention. In the entire cohort, there were no significant differences in changes in DI, HOMA2%Scpep, or C-peptide response between the 2 groups. Among participants with baseline 25(OH)D level &amp;lt;12 ng\/mL, the mean percent differences for DI between the vitamin D and placebo groups was 8.5 (95% CI, 0.2-16.8).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>Supplementation with vitamin D3 for 24 months did not improve an OGTT-derived index of \u03b2-cell function in people with prediabetes not selected based on baseline vitamin D status; however, there was benefit among those with very low baseline vitamin D status.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1210\/clinem\/dgab649","type":"journal-article","created":{"date-parts":[[2021,9,2]],"date-time":"2021-09-02T15:11:33Z","timestamp":1630595493000},"page":"230-240","source":"Crossref","is-referenced-by-count":54,"title":["Effects of Vitamin D Supplementation on Insulin Sensitivity and Secretion in Prediabetes"],"prefix":"10.1210","volume":"107","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1269-3580","authenticated-orcid":false,"given":"Neda","family":"Rasouli","sequence":"first","affiliation":[{"name":"Division of Endocrinology, Metabolism and Diabetes, University of Colorado School of Medicine and VA Eastern Colorado Health Care System, Aurora, CO 80045, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Irwin G","family":"Brodsky","sequence":"additional","affiliation":[{"name":"Endocrinology and Diabetes Center, Maine Medical Center and Maine Medical Center Research Institute, Scarborough, ME 04101, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4294-8081","authenticated-orcid":false,"given":"Ranee","family":"Chatterjee","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke University, Durham, NC 27713, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sun H","family":"Kim","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Gerontology and Metabolism, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard E","family":"Pratley","sequence":"additional","affiliation":[{"name":"AdventHealth Translational Research Institute, Orlando, FL 32804, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Myrlene A","family":"Staten","sequence":"additional","affiliation":[{"name":"National Institute of Diabetes and Digestive, and Kidney Diseases, Bethesda, MD 20892 (retired), USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0124-7174","authenticated-orcid":false,"given":"Anastassios G","family":"Pittas","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Metabolism, Tufts Medical Center, Boston, MA 02111, 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