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We have reported that extracellular nicotinamide phosphoribosyltransferase (eNAMPT) is elevated in type 2 diabetes and that elevated eNAMPT levels promote beta-cell dysfunction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To further investigate the effects of eNAMPT on beta-cell mass.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Islets isolated from CD1 and Ins1tm1.1(cre)Thor+\/\u2212; mTmGfl\/\u2212 mice and human donors were exposed to eNAMPT (48-96\u2005hours). CD1 mice were administered eNAMPT for 14 days. Alpha-, beta-, and delta-cell numbers were determined by glucagon, insulin, and somatostatin staining, respectively. Alpha-cell proliferation was assessed by bromodeoxyuridine (BrDU) uptake and Ki67 expression. Glucagon secretion was assessed via radioimmunoassay. Trans-differentiation was assessed by determining changes in presence of bi-hormonal cells in CD1\/human islets and using Ins1tm1.1(cre)Thor+\/\u2212; mTmGfl\/\u2212 islets to determine changes in GLU+\/GFP+ and GLU+\/TdT+ cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>eNAMPT treatment reduced beta-cell number and induced corresponding increases in alpha-cell number. Indicative of beta- to alpha-cell trans-differentiation eNAMPT induced increased presence of bi-hormonal INS+\/GLU+ cells and PDX1+\/GLU+ cells, and increased GLU+\/GFP+ cells in Ins1tm1.1(cre)Thor+\/\u2212; mTmGfl\/\u2212 mouse islets. In addition, eNAMPT induced alpha-cell proliferation, indicated by increased BrDU uptake. Despite marked elevation in alpha-cell number, alpha-cell function was compromised following eNAMPT exposure, indicated by impaired glucagon counterregulatory response (CCR) to low glucose levels.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This data supports a role for elevated eNAMPT levels in driving increased alpha-cell mass via a combination of beta- to alpha-cell trans-differentiation and alpha-cell proliferation. When combined with observed impaired CCR, these data have implications for both type 1 and type 2 diabetes pathophysiology.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1210\/endocr\/bqag061","type":"journal-article","created":{"date-parts":[[2026,6,5]],"date-time":"2026-06-05T11:46:34Z","timestamp":1780659994000},"source":"Crossref","is-referenced-by-count":0,"title":["eNAMPT induces alpha-cell mass expansion but impaired glucagon counter regulatory response"],"prefix":"10.1210","volume":"167","author":[{"given":"Sophie R","family":"Sayers","sequence":"first","affiliation":[{"name":"Diabetes and Obesity Theme, School of Cardiovascular and Metabolic Medicine & Sciences, King's College London , London SE1 1UL ,","place":["UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vesela S","family":"Gesheva","sequence":"additional","affiliation":[{"name":"Diabetes and Obesity Theme, School of Cardiovascular and Metabolic Medicine & Sciences, King's College London , 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