{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T13:56:58Z","timestamp":1772632618844,"version":"3.50.1"},"reference-count":61,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T00:00:00Z","timestamp":1772582400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell Dev. Biol."],"abstract":"<jats:sec>\n                    <jats:title>Purpose<\/jats:title>\n                    <jats:p>DNA replication helicase\/nuclease 2 (DNA2) is an evolutionarily conserved nuclease-helicase with known role in maintaining nuclear genome stability. However, its potential involvement in metabolic regulation and disease remains unclear. This study investigates the role of DNA2 in pancreatic \u03b2 cell physiology and diabetes pathogenesis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      \u03b2 cell-specific DNA2 knockout mice (DNA2\n                      <jats:sup>INS2\u2212\/\u2212<\/jats:sup>\n                      ) were generated and fed either a chow diet (CD) or high-fat diet (HFD). Metabolic phenotyping, insulin secretion assays, transcriptomic profiling, mitochondrial function analysis, and ultrastructural imaging were performed. INS-1 cells were used to assess the functions of DNA2\n                      <jats:italic>in vitro<\/jats:italic>\n                      through knockdown, overexpression and site-directed mutagenesis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      DNA2\n                      <jats:sup>INS2\u2212\/\u2212<\/jats:sup>\n                      mice exhibited normal metabolic profiles under CD, but developed severe hyperglycemia, hyperinsulinemia, insulin resistance, and ectopic lipid deposition upon HFD feeding. This phenotype was accompanied by increased \u03b2 cell proliferation and glucose-stimulated insulin secretion. RNA sequencing revealed the dysregulation of mitochondrial regulatory genes in DNA2-deficient islets. Functional assays confirmed that DNA2 deletion enhanced mitochondrial ATP production and oxidative phosphorylation, whereas its overexpression suppressed mitochondrial activity. Domain-specific mutagenesis demonstrated that both nuclease and helicase activities are essential for DNA2-mediated metabolic regulation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our findings identify DNA2 as a negative regulator of mitochondrial bioenergetics and insulin secretion in \u03b2 cells. By limiting mitochondrial activity, DNA2 serves as a rheostat that prevents \u03b2 cell overactivation during metabolic stress, thereby preserving systemic glucose homeostasis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fcell.2026.1733190","type":"journal-article","created":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T07:02:55Z","timestamp":1772607775000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["DNA2 acts as a brake on \u03b2 cell insulin hypersecretion and diet-induced metabolic dysfunction"],"prefix":"10.3389","volume":"14","author":[{"given":"Haixia","family":"Xu","sequence":"first","affiliation":[{"name":"State Key Laboratory of Biotherapy and Cancer Center, Department of Pharmacy, Institute of Metabolic Diseases and Pharmacotherapy, West China Hospital, Sichuan University","place":["Chengdu, Sichuan, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dongmei","family":"Tang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Biotherapy and Cancer Center, Department of Biotherapy, Center for Diabetes and Metabolism Research, West China Hospital, Sichuan University","place":["Chengdu, Sichuan, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Na","family":"Yang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Biotherapy and Cancer Center, Department of Pharmacy, Institute of Metabolic Diseases and Pharmacotherapy, West China Hospital, Sichuan University","place":["Chengdu, Sichuan, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Meilin","family":"Ma","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Biotherapy and Cancer Center, Department of Pharmacy, Institute of Metabolic Diseases and Pharmacotherapy, West China Hospital, Sichuan University","place":["Chengdu, Sichuan, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yan","family":"Tian","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Biotherapy and Cancer Center, Department of Biotherapy, Center for Diabetes and Metabolism Research, West China Hospital, Sichuan University","place":["Chengdu, Sichuan, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xianghui","family":"Fu","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Biotherapy and Cancer Center, Department of Biotherapy, Center for Diabetes and Metabolism Research, West China Hospital, Sichuan University","place":["Chengdu, Sichuan, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1965","published-online":{"date-parts":[[2026,3,4]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"413","DOI":"10.1038\/s41574-025-01114-y","article-title":"Insulin resistance in type 2 diabetes mellitus","volume":"21","author":"Accili","year":"2025","journal-title":"Nat. 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