{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,13]],"date-time":"2026-01-13T16:22:50Z","timestamp":1768321370135,"version":"3.49.0"},"reference-count":67,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2018,9,14]],"date-time":"2018-09-14T00:00:00Z","timestamp":1536883200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"},{"start":{"date-parts":[[2018,9,14]],"date-time":"2018-09-14T00:00:00Z","timestamp":1536883200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["asbmr.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2019,1,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:sec>\n                  <jats:title>\u2003<\/jats:title>\n                  <jats:p>Despite increased longevity and resistance to multiple stressors, growth hormone receptor null (GHRKO) mice exhibit severe skeletal impairment. The role of GHR in maintaining osteocyte mitochondrial function is unknown. We found that GHR ablation was detrimental to osteocyte mitochondrial function. In vivo multiphoton microscopy revealed significant reductions of &amp;gt;10% in mitochondrial membrane potential (MMP) in GHRKO osteocytes and reduced mitochondrial volumetric density. Reductions in MMP were accompanied by reductions in glucose transporter-1 levels, steady state ATP, NADH redox index, oxygen consumption rate, and mitochondrial reserve capacity in GHRKO osteocytes. Glycolytic capacity did not differ between control and GHRKO males\u2019 osteocytes. However, osteocytes from aged female GHRKO mice exhibited reductions in glycolytic parameters, indicating impairments in glucose metabolism, which may be sex dependent. GHRKO osteocytes exhibited increased levels of cytoplasmic reactive oxygen species (ROS) (both basal and in response to high glucose), insulin-like growth factor-1 (IGF-1), and insulin. Mitochondrial ROS levels were increased and correlated with reduced glutathione in GHRKO osteocytes. Overall, the compromised osteocyte mitochondrial function and responses to metabolic insults strongly correlated with skeletal impairments, suggesting that despite increased life span of the GHRKO mice, skeletal health span is decreased. \u00a9 2018 American Society for Bone and Mineral Research.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1002\/jbmr.3573","type":"journal-article","created":{"date-parts":[[2018,9,16]],"date-time":"2018-09-16T09:53:28Z","timestamp":1537091608000},"page":"106-122","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["Mitochondrial Function Is Compromised in Cortical Bone Osteocytes of Long-Lived Growth Hormone Receptor Null Mice"],"prefix":"10.1093","volume":"34","author":[{"given":"Zhongbo","family":"Liu","sequence":"first","affiliation":[{"name":"David B. Kriser Dental CenterDepartment of Basic Science and Craniofacial BiologyNew York University College of DentistryNew YorkNYUSA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maria E","family":"Solesio","sequence":"additional","affiliation":[{"name":"David B. Kriser Dental CenterDepartment of Basic Science and Craniofacial BiologyNew York University College of DentistryNew YorkNYUSA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mitchell B","family":"Schaffler","sequence":"additional","affiliation":[{"name":"Department of Biomedical EngineeringCity College of New YorkNew YorkNYUSA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dorra","family":"Frikha-Benayed","sequence":"additional","affiliation":[{"name":"Department of Biomedical EngineeringCity College of New YorkNew YorkNYUSA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Clifford J","family":"Rosen","sequence":"additional","affiliation":[{"name":"Maine Medical Center Research InstituteScarboroughMEUSA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Haim","family":"Werner","sequence":"additional","affiliation":[{"name":"Department of Human Molecular Genetics and BiochemistrySackler School of MedicineTel Aviv UniversityTel AvivIsrael"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John J","family":"Kopchick","sequence":"additional","affiliation":[{"name":"Edison Biotechnology Institute and Department of Biomedical SciencesOhio UniversityAthensOHUSA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Evgeny V","family":"Pavlov","sequence":"additional","affiliation":[{"name":"David B. Kriser Dental CenterDepartment of Basic Science and Craniofacial BiologyNew York University College of DentistryNew YorkNYUSA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrey Y","family":"Abramov","sequence":"additional","affiliation":[{"name":"Department of Molecular NeuroscienceUCL Institute of NeurologyQueen SquareLondonUK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shoshana","family":"Yakar","sequence":"additional","affiliation":[{"name":"David B. 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