{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T17:04:04Z","timestamp":1786122244193,"version":"build-2736575974"},"reference-count":119,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2026,6,28]],"date-time":"2026-06-28T00:00:00Z","timestamp":1782604800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,6,28]],"date-time":"2026-06-28T00:00:00Z","timestamp":1782604800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["dom-pubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Diabetes Obesity Metabolism"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Preadipocyte commitment to the adipogenic lineage declines markedly with advancing age, while triglyceride accumulation in hypertrophied existing adipocytes persists or expands. This creates a dissociation between adipogenic capacity and lipid\u2010buffering demand, progressively weakening depot metabolic competence and contributing to systemic insulin resistance.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>This review examines the molecular mechanisms linking impaired adipose tissue plasticity during ageing to metabolic decline, and appraises therapeutic strategies that may restore adipose progenitor competence or limit downstream metabolic dysfunction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Findings<\/jats:title>\n                    <jats:p>\n                      Ageing adipose tissue is characterized by four interlocking defects. First, transcriptional reprogramming, including induction of the inhibitory CCAAT\/enhancer\u2010binding protein \u03b2\u2010LIP isoform through CUG triplet repeat\u2010binding protein 1, together with reduced C\/EBP\u03b1 and peroxisome proliferator\u2010activated receptor \u03b3 activity, shifts progenitors away from differentiation and toward hypertrophic lipid storage. Second, SIRT7 opposes SIRT1 in regulating adipogenic commitment, implicating sirtuin and NAD\n                      <jats:sup>+<\/jats:sup>\n                      dysregulation in the age\u2010related adipogenic deficit. Third, nuclear lamina remodelling restricts chromatin accessibility at adipogenic loci. Fourth, senescent cells accumulate in ageing depots and generate a senescence\u2010associated secretory phenotype enriched in interleukin\u20106, tumour necrosis factor\u2010\u03b1, and matrix metalloproteinases, sustaining local inflammation and inhibiting preadipocyte differentiation. These changes occur alongside redistribution of fat from subcutaneous depots toward visceral, hepatic, muscular, and perivascular compartments, accelerating insulin resistance, Type 2 diabetes, and cardiovascular disease. Sex\u2010specific depot trajectories diverge, and rodent models reproduce these patterns only partly.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Therapeutic Implications<\/jats:title>\n                    <jats:p>\n                      Senolytics, NAD\n                      <jats:sup>+<\/jats:sup>\n                      precursors, and incretin\u2010based agents, including GLP\u20101 and dual GIP\/GLP\u20101 receptor agonists, are reviewed together with still\u2010preclinical stem cell and CRISPR approaches, ranked by translational readiness.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Restoring adipose progenitor competence while preserving depot\u2010specific metabolic identity may help slow age\u2010related metabolic deterioration and prolong healthspan.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/dom.71037","type":"journal-article","created":{"date-parts":[[2026,6,29]],"date-time":"2026-06-29T02:26:06Z","timestamp":1782699966000},"page":"7752-7767","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The Ageing Adipose Paradox: Implications for Metabolic Health"],"prefix":"10.1111","volume":"28","author":[{"given":"Dana Bou","family":"Matar","sequence":"first","affiliation":[{"name":"Department of Physiology, College of Medicine Alfaisal University  Riyadh Saudi Arabia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Muhammad Affan","family":"Elahi","sequence":"additional","affiliation":[{"name":"College of Medicine Alfaisal University  Riyadh Saudi Arabia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-2148-0006","authenticated-orcid":false,"given":"Walid Khaled","family":"Nassar","sequence":"additional","affiliation":[{"name":"College of Medicine Alfaisal University  Riyadh Saudi Arabia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohammed I.","family":"Alotaibi","sequence":"additional","affiliation":[{"name":"Bristol Medical School: Translational Health Sciences University of Bristol, Dorothy Hodgkin Building  Bristol UK"},{"name":"Department of Medical Biochemistry, College of Medicine Taif University  Taif Saudi Arabia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Murphy","sequence":"additional","affiliation":[{"name":"College of Medicine Alfaisal University  Riyadh Saudi Arabia"},{"name":"Bristol Medical School: Translational Health Sciences University of Bristol, Dorothy Hodgkin Building  Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hana M. 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