{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T23:54:30Z","timestamp":1792194870741,"version":"4.4.0"},"reference-count":55,"publisher":"The Endocrine Society","issue":"10","license":[{"start":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:00:00Z","timestamp":1787011200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"name":"VA Merit Review","award":["1I01BX002567"],"award-info":[{"award-number":["1I01BX002567"]}]},{"DOI":"10.13039\/501100012264","name":"NIH","doi-asserted-by":"publisher","award":["P20GM144269"],"award-info":[{"award-number":["P20GM144269"]}],"id":[{"id":"10.13039\/501100012264","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100012264","name":"NIH","doi-asserted-by":"publisher","award":["T32DK128770"],"award-info":[{"award-number":["T32DK128770"]}],"id":[{"id":"10.13039\/501100012264","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100012264","name":"NIH","doi-asserted-by":"publisher","award":["T32AG07811"],"award-info":[{"award-number":["T32AG07811"]}],"id":[{"id":"10.13039\/501100012264","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,9,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Liver-specific ER\u03b1 knockout (LERKO) mice with normal ovarian function are not susceptible to steatosis and maintain mitochondrial function. Here, we tested whether loss of hepatic ER\u03b1 blunts estrogen modulation of hepatic mitochondrial respiratory capacity and mitochondrial proteome following ovariectomy (OVX). Sham or OVX surgery was performed in middle-aged female mice (36-40 weeks), followed by adeno-associated virus (AAV) injection to generate Control (Con; green fluorescent protein) or LERKO mice (Cre). All mice were placed on a high-fat diet for 10 weeks following surgery. Half of the OVX mice received 17\u03b2-estradiol (E2) replacement (OVX + E2) for the last 4 weeks. OVX mice had greater body mass and adiposity, which was reversed by E2 replacement in both Con and LERKO mice. E2 replacement reduced steatosis in both Con and LERKO OVX mice, but the LERKO OVX mice maintained greater hepatic triglycerides. E2 replacement promoted greater basal and ADP\u2013stimulated (State 3) mitochondrial respiration in Con OVX but not in LERKO OVX mice. Changes in mitochondrial respiration could not be attributed to altered responses to changes in energy demand (GATP) or to alterations in mitochondrial H2O2 production. Conversely, maximal coupled branched-chain amino acid\u2013supported respiration was universally suppressed by E2 replacement. Proteomics analysis revealed E2-mediated reductions in hepatic mitochondrial energy transduction in both Con and LERKO mice. In conclusion, post\u2013OVX estrogen treatment reduces steatosis in the absence of hepatic ER\u03b1; however, steatosis remains higher, and mitochondrial deficits persist despite similar proteomic changes, suggesting ER\u03b1 is required for optimal response to estrogen in modulating hepatic mitochondrial respiration.<\/jats:p>","DOI":"10.1210\/endocr\/bqag093","type":"journal-article","created":{"date-parts":[[2026,8,14]],"date-time":"2026-08-14T11:32:45Z","timestamp":1786707165000},"source":"Crossref","is-referenced-by-count":2,"title":["Hepatocyte ER\u03b1 mediates estrogen-induced augmentation of hepatic mitochondrial respiration following ovariectomy"],"prefix":"10.1210","volume":"167","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0845-4002","authenticated-orcid":false,"given":"Edziu","family":"Franczak","sequence":"first","affiliation":[{"name":"Department of Cell Biology and Physiology, The University of Kansas Medical Center , Kansas City, KS 66160 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City, MO 64128 ,","place":["USA"]},{"name":"Kansas Center for Metabolism and Obesity Research , The University of Kansas Medical Center, Kansas City, KS 66160 ,","place":["USA"]},{"name":"KU Diabetes Institute and Department of Internal Medicine, Division of Endocrinology, The University of Kansas Medical Center , Kansas City, KS 66160 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7046-3623","authenticated-orcid":false,"given":"Edward Matthew","family":"Morris","sequence":"additional","affiliation":[{"name":"Department of Cell Biology and Physiology, The University of Kansas Medical Center , Kansas City, KS 66160 ,","place":["USA"]},{"name":"Kansas Center for Metabolism and Obesity Research , The University of Kansas Medical Center, Kansas City, KS 66160 ,","place":["USA"]},{"name":"KU Diabetes Institute and Department of Internal Medicine, Division of Endocrinology, The University of Kansas Medical Center , Kansas 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