{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T17:16:57Z","timestamp":1792603017995,"version":"4.5.0"},"reference-count":18,"publisher":"The Endocrine Society","issue":"4","license":[{"start":{"date-parts":[[2020,2,11]],"date-time":"2020-02-11T00:00:00Z","timestamp":1581379200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"AstraZeneca Pharmaceuticals LP","award":["10400"],"award-info":[{"award-number":["10400"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Context<\/jats:title>\n                  <jats:p>Dapagliflozin and other SGLT2 inhibitors are known to increase hematocrit, possibly due to its diuretic effects and hemoconcentration.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Objective<\/jats:title>\n                  <jats:p>Since type 2 diabetes is a proinflammatory state and since hepcidin, a known suppressor of erythropoiesis, is increased in proinflammatory states, we investigated the possibility that dapagliflozin suppresses hepcidin concentrations and thus increases erythropoiesis.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Design<\/jats:title>\n                  <jats:p>Prospective, randomized, and placebo-controlled study.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Setting<\/jats:title>\n                  <jats:p>Single endocrinology center.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Patients<\/jats:title>\n                  <jats:p>Fifty-two obese type 2 diabetes patients.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Intervention<\/jats:title>\n                  <jats:p>Patients were randomized (1:1) to either dapagliflozin (10 mg daily) or placebo for 12 weeks. Blood samples were collected before and after treatments and serum, plasma, and mononuclear cells (MNC) were prepared.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Main Outcome Measure<\/jats:title>\n                  <jats:p>Hepcidin and other hematopoietic factors.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>Following dapagliflozin treatment, there was a significant fall in HbA1c and a significant increase in hemoglobin concentration and hematocrit. Dapagliflozin treatment significantly reduced circulating hepcidin and ferritin concentrations while causing a significant increase in levels of the hepcidin inhibitor, erythroferrone, and a transient increase in erythropoietin. Additionally, dapagliflozin increased plasma transferrin levels and expression of transferrin receptors 1 and 2 in MNC, while there was no change in the expression of the iron cellular transporter, ferroportin. Dapagliflozin treatment also caused a decrease in hypoxia-induced factor-1\u03b1 expression in MNC while it increased the expression of its inhibitor, prolyl hydroxylase-2. There were no significant changes in any of these indices in the placebo group.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>We conclude that dapagliflozin increases erythropoiesis and hematocrit through mechanisms that involve the suppression of hepcidin and the modulation of other iron regulatory proteins.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1210\/clinem\/dgaa057","type":"journal-article","created":{"date-parts":[[2020,2,11]],"date-time":"2020-02-11T14:26:25Z","timestamp":1581431185000},"page":"e1056-e1063","source":"Crossref","is-referenced-by-count":175,"title":["Dapagliflozin Suppresses Hepcidin And Increases Erythropoiesis"],"prefix":"10.1210","volume":"105","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6333-6033","authenticated-orcid":false,"given":"Husam","family":"Ghanim","sequence":"first","affiliation":[{"name":"Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanaa","family":"Abuaysheh","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeanne","family":"Hejna","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kelly","family":"Green","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manav","family":"Batra","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antione","family":"Makdissi","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ajay","family":"Chaudhuri","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paresh","family":"Dandona","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"80","published-online":{"date-parts":[[2020,2,11]]},"reference":[{"issue":"12","key":"2021122209564172500_CIT0001","doi-asserted-by":"crossref","first-page":"844","DOI":"10.14740\/jocmr2760w","article-title":"Increased hematocrit during sodium-glucose cotransporter 2 inhibitor therapy indicates recovery of tubulointerstitial function in diabetic kidneys","volume":"8","author":"Sano","year":"2016","journal-title":"J Clin Med 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