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The large MAF transcription factor MAFB is expressed in human \u03b1- and \u03b2-cells, marks their most functionally mature subpopulations, and is downregulated in diabetes, but its role in adult human islets has not been tested directly. Using shRNA-mediated MAFB knockdown (KD) in whole and CD26\n                  <jats:sup>+<\/jats:sup>\n                  \u03b1-cell-enriched human pseudoislets, we found that whole pseudoislet MAFB KD impaired glucagon synthesis and secretion while only modestly reducing insulin content and cAMP-potentiated insulin release. Single-cell profiling detected no \u03b2-cell transcriptional response beyond MAFB KD itself, consistent with buffering by the related \u03b2-cell-enriched MAFA transcription factor. In contrast, \u03b1-cell-restricted MAFB KD unmasked a cell-autonomous requirement for MAFB in stimulus-secretion coupling. MAFB deficiency also destabilized \u03b1-cell identity, downregulating canonical \u03b1-cell and neuroendocrine secretory genes while ectopically inducing mesenchymal and extracellular matrix remodeling programs. In addition, MAFB-dependent downregulation of electron transport chain genes was confined to a large \u03b1-cell subcluster, manifesting as impaired islet-wide mitochondrial respiration within the broader \u03b1-cell population. Together, these findings identify MAFB as an essential adult human \u03b1-cell maintenance factor that links diabetes-associated downregulation to impaired glucagon secretion, \u03b1-cell identity erosion, and mitochondrial dysfunction.\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>RESEARCH IN CONTEXT<\/jats:title>\n                  <jats:list list-type=\"bullet\">\n                    <jats:list-item>\n                      <jats:p>\n                        <jats:bold>What is already known about this subject?<\/jats:bold>\n                        <jats:list list-type=\"bullet\">\n                          <jats:list-item>\n                            <jats:p>MAFB is expressed in adult human \u03b1- and \u03b2-cells, marks their most functionally mature subpopulations, and is downregulated in type 1 and type 2 diabetes<\/jats:p>\n                          <\/jats:list-item>\n                          <jats:list-item>\n                            <jats:p>In human stem cell models, MAFB is essential for generating insulin-producing \u03b2-like cells, whereas glucagon-producing \u03b1-like cells are reduced but still formed<\/jats:p>\n                          <\/jats:list-item>\n                          <jats:list-item>\n                            <jats:p>Neither model addresses adult human islets: rodent MafB becomes \u03b1-cell restricted after birth, and stem cell models capture differentiation, not maintenance<\/jats:p>\n                          <\/jats:list-item>\n                        <\/jats:list>\n                      <\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>\n                        <jats:bold>What is the key question?<\/jats:bold>\n                        <jats:list list-type=\"bullet\">\n                          <jats:list-item>\n                            <jats:p>Is MAFB required to maintain identity and secretory function in adult human islet cells?<\/jats:p>\n                          <\/jats:list-item>\n                        <\/jats:list>\n                      <\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>\n                        <jats:bold>What are the new findings?<\/jats:bold>\n                        <jats:list list-type=\"bullet\">\n                          <jats:list-item>\n                            <jats:p>MAFB knockdown in primary human pseudoislets impaired glucagon synthesis and secretion but minimally affected \u03b2-cells, consistent with buffering by MAFA<\/jats:p>\n                          <\/jats:list-item>\n                          <jats:list-item>\n                            <jats:p>Knockdown in CD26+ \u03b1-cell-enriched pseudoislets revealed a cell-autonomous requirement for MAFB in stimulus-secretion coupling, and destabilized \u03b1-cell identity by inducing mesenchymal and extracellular matrix programs<\/jats:p>\n                          <\/jats:list-item>\n                          <jats:list-item>\n                            <jats:p>MAFB loss downregulated electron transport chain genes in the largest \u03b1-cell subcluster and reduced mitochondrial respiration<\/jats:p>\n                          <\/jats:list-item>\n                        <\/jats:list>\n                      <\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>\n                        <jats:bold>How might this impact on clinical practice in the foreseeable future?<\/jats:bold>\n                        <jats:list list-type=\"bullet\">\n                          <jats:list-item>\n                            <jats:p>Preserving MAFB activity in adult human \u03b1-cells may represent a strategy to limit \u03b1-cell dysfunction in diabetes<\/jats:p>\n                          <\/jats:list-item>\n                        <\/jats:list>\n                      <\/jats:p>\n                    <\/jats:list-item>\n                  <\/jats:list>\n                <\/jats:sec>","DOI":"10.64898\/2026.08.08.743687","type":"posted-content","created":{"date-parts":[[2026,8,14]],"date-time":"2026-08-14T18:15:17Z","timestamp":1786731317000},"source":"Crossref","is-referenced-by-count":0,"title":["MAFB is essential for the maintenance of adult human \u03b1-cell identity and glucagon secretion"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6604-3906","authenticated-orcid":false,"given":"KC","family":"Coate","sequence":"first","affiliation":[{"name":"Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN"},{"name":"Department of Medicine, Division of Diabetes, Endocrinology and Metabolism, Vanderbilt University Medical Center, Nashville, TN"},{"name":"Department of Veterans Affairs, Tennessee Valley Healthcare System, Nashville, 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