{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T22:36:20Z","timestamp":1788820580803,"version":"build-2803163510"},"reference-count":59,"publisher":"SAGE Publications","issue":"4-6","license":[{"start":{"date-parts":[[2022,8,1]],"date-time":"2022-08-01T00:00:00Z","timestamp":1659312000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Antioxidants &amp; Redox Signaling"],"published-print":{"date-parts":[[2022,8]]},"abstract":"<jats:sec>\n                    <jats:title>Aims:<\/jats:title>\n                    <jats:p>\n                      The skeletal muscle maintains glucose disposal\n                      <jats:italic toggle=\"yes\">via<\/jats:italic>\n                      insulin signaling and glucose transport. The progression of diabetes and insulin resistance is critically influenced by endoplasmic reticulum (ER) stress.\n                      <jats:sc>d<\/jats:sc>\n                      -Allulose, a low-calorie sugar substitute, has shown crucial physiological activities under conditions involving hyperglycemia and insulin resistance. However, the molecular mechanisms of\n                      <jats:sc>d<\/jats:sc>\n                      -allulose in the progression of diabetes have not been fully elucidated. Here, we evaluated the effect of\n                      <jats:sc>d<\/jats:sc>\n                      -allulose on hyperglycemia-associated ER stress responses in human skeletal myoblasts (HSkM) and\n                      <jats:italic toggle=\"yes\">db\/db<\/jats:italic>\n                      diabetic and high-fat diet-fed mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      <jats:sc>d<\/jats:sc>\n                      -allulose effectively controlled glycemic markers such as insulin and hemoglobin A1c (HbA1c), showing anti-diabetic effects by inhibiting the disruption of insulin receptor substrate (IRS)-1 tyrosine phosphorylation and glucose transporter 4 (GLUT4) expression, in which the phosphatidylinositol-3 kinase (PI3K)\/protein kinase B (Akt) pathway is involved. The levels of glucose dysmetabolism-based NADPH oxidase, such as NADPH-dependent oxidoreductase (Nox) 4, were highly increased, and their interaction with IRE1\u03b1 and the resultant sulfonation-regulated IRE1-dependent decay (RIDD)-\n                      <jats:italic toggle=\"yes\">Sirt1<\/jats:italic>\n                      decay were also highly increased under diabetic conditions, which were controlled with\n                      <jats:sc>d<\/jats:sc>\n                      -allulose treatment. Skeletal muscle cells grown with a high glucose medium supplemented with\n                      <jats:sc>d<\/jats:sc>\n                      -allulose showed controlled IRE1\u03b1 sulfonation-RIDD-\n                      <jats:italic toggle=\"yes\">Sirt1<\/jats:italic>\n                      decay, in which Nox4 was involved.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Innovation and Conclusion:<\/jats:title>\n                    <jats:p>\n                      The study observations indicate that\n                      <jats:sc>d<\/jats:sc>\n                      -allulose contributes to the muscular glucose disposal in the diabetic state where ER-localized Nox4-induced IRE1\u03b1 sulfonation results in the decay of\n                      <jats:italic toggle=\"yes\">Sirt1<\/jats:italic>\n                      , a core factor for controlling glucose metabolism.\n                      <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                      37, 229\u2013245.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1089\/ars.2021.0207","type":"journal-article","created":{"date-parts":[[2022,2,15]],"date-time":"2022-02-15T06:23:13Z","timestamp":1644906193000},"page":"229-245","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":14,"title":["<scp>d<\/scp>\n                    -Allulose Ameliorates Hyperglycemia Through IRE1\u03b1 Sulfonation-RIDD-\n                    <i>Sirt1<\/i>\n                    Decay Axis in the Skeletal Muscle"],"prefix":"10.1177","volume":"37","author":[{"given":"Hwa-Young","family":"Lee","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Institute of New Drug Development, Jeonbuk National University Medical School, Jeonju, South Korea."},{"name":"Non-Clinical Evaluation Center Biomedical Research Institute, Jeonbuk National University Hospital, Jeonju, South Korea."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Geum-Hwa","family":"Lee","sequence":"additional","affiliation":[{"name":"Non-Clinical Evaluation Center Biomedical Research Institute, Jeonbuk National University Hospital, Jeonju, South Korea."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"The-Hiep","family":"Hoang","sequence":"additional","affiliation":[{"name":"Non-Clinical Evaluation Center Biomedical Research Institute, Jeonbuk National University Hospital, Jeonju, South Korea."},{"name":"Research Institute of Clinical Medicine of Jeonbuk National University-Biomedical Research Institute of Jeonbuk National University Hospital, Jeonju, South Korea."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seon-Ah","family":"Park","sequence":"additional","affiliation":[{"name":"Non-Clinical Evaluation Center Biomedical Research Institute, Jeonbuk National University Hospital, Jeonju, South Korea."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juwon","family":"Lee","sequence":"additional","affiliation":[{"name":"School of Pharmacy, Jeonbuk National University, Jeonju, South Korea."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junghyun","family":"Lim","sequence":"additional","affiliation":[{"name":"School of Pharmacy, Jeonbuk National University, Jeonju, South Korea."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Soonok","family":"Sa","sequence":"additional","affiliation":[{"name":"Food Biotech R&amp;D Center, Samyang Corp., Seongnam-si, South Korea."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Go Eun","family":"Kim","sequence":"additional","affiliation":[{"name":"Food Biotech R&amp;D Center, Samyang Corp., Seongnam-si, South Korea."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jung Sook","family":"Han","sequence":"additional","affiliation":[{"name":"Food Biotech R&amp;D Center, Samyang Corp., Seongnam-si, South Korea."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junghyun","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Oral Pathology, School of Dentistry, Jeonbuk National University, Jeonju, South Korea."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4190-9889","authenticated-orcid":false,"given":"Han-Jung","family":"Chae","sequence":"additional","affiliation":[{"name":"Non-Clinical Evaluation Center Biomedical Research Institute, Jeonbuk National University Hospital, Jeonju, South Korea."},{"name":"School of Pharmacy, Jeonbuk National University, Jeonju, South 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