{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T12:18:17Z","timestamp":1788178697734,"version":"build-2803163510"},"reference-count":57,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2026,8,10]],"date-time":"2026-08-10T00:00:00Z","timestamp":1786320000000},"content-version":"vor","delay-in-days":9,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,8,1]],"date-time":"2026-08-01T00:00:00Z","timestamp":1785542400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AA018282"],"award-info":[{"award-number":["AA018282"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100014517","name":"Louisiana Biomedical Research Network","doi-asserted-by":"publisher","award":["P20GM103424"],"award-info":[{"award-number":["P20GM103424"]}],"id":[{"id":"10.13039\/100014517","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000001","name":"National Science Foundation","doi-asserted-by":"publisher","award":["2349224"],"award-info":[{"award-number":["2349224"]}],"id":[{"id":"10.13039\/100000001","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Alcohol, Clinical and Experimental Research"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Alcohol consumption and aging are factors promoting osteopenia and osteoporosis. How these factors interact is poorly understood. To investigate this relationship, a binge ethanol exposure model in mice was used to determine how aging affects skeletal responses to binge ethanol.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Dmp1\u2010Cre TdTomato mice with the fluorescent marker TdTomato expressed in osteoblasts and osteocytes, and control mice without Cre expression were used. Mice of both sexes at 12\u2009weeks and 78\u2009weeks of age were gavaged for four consecutive days with 3, 3, 4, and 4.5\u2009g of ethanol\/kg of body weight or with PBS (control). Skeletal responses were determined by serum bone turnover markers using ELISA and by gene expression and protein measurement in the femoral shaft and lumbar vertebrae using qRT\u2010PCR and western blots.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Ethanol and aging both significantly decreased serum levels of Procollagen Type I (P1NP) and osteocalcin, indicating reduced bone formation. Serum levels of C\u2010terminal telopeptide of type I collagen (CTX\u20101) increased significantly with ethanol exposure in the aging mice, reflecting enhanced bone resorption. In the femoral shaft, ethanol and aging increased the expression of genes involved in osteoclast activation, Calcitonin receptor (Calcr) and RANKL, with a significantly larger induction of receptor activator of nuclear factor\u2010\u03baB ligand (RANKL) mRNA in 78\u2010week\u2010old than 12\u2010week\u2010old mice. Expression of osteoblast\u2010associated genes, Collagen Type I Alpha 1 Chain (Col1a1), Collagen Type I Alpha 2 Chain (Col1a2), and Sphingomyelin phosphodiesterase 3 (Smpd3), was downregulated by ethanol, with stronger ethanol\u2010mediated reduction in the 78\u2010week\u2010old than 12\u2010week\u2010old mice. Aging did not decrease the expression of TdTomato mRNA or TdTomato protein, indicating no overall loss of osteoblasts and osteocytes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Binge ethanol exposure and aging independently and synergistically disrupt bone remodeling by inhibiting bone formation and enhancing bone resorption.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/acer.70384","type":"journal-article","created":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T04:03:27Z","timestamp":1786421007000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Aging Exacerbates Binge Ethanol\u2010Mediated Bone Toxicity in Mice"],"prefix":"10.1111","volume":"50","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3122-4635","authenticated-orcid":false,"given":"Kim 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