{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T16:24:53Z","timestamp":1787588693294,"version":"build-2736575974"},"reference-count":73,"publisher":"The Endocrine Society","issue":"6","license":[{"start":{"date-parts":[[2022,4,21]],"date-time":"2022-04-21T00:00:00Z","timestamp":1650499200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["RO1 DK084842"],"award-info":[{"award-number":["RO1 DK084842"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["T32 HL007249"],"award-info":[{"award-number":["T32 HL007249"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100005825","name":"National Institute of Food and Agriculture","doi-asserted-by":"publisher","award":["2015\u201303545"],"award-info":[{"award-number":["2015\u201303545"]}],"id":[{"id":"10.13039\/100005825","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,6,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Placental insufficiency (PI) lowers fetal oxygen and glucose concentrations, which disrupts glucose-insulin homeostasis and promotes fetal growth restriction (FGR). To date, prenatal treatments for FGR have not attempted to correct the oxygen and glucose supply simultaneously. Therefore, we investigated whether a 5-day correction of oxygen and glucose concentrations in PI-FGR fetuses would normalize insulin secretion and glucose metabolism. Experiments were performed in near-term FGR fetal sheep with maternal hyperthermia-induced PI. Fetal arterial oxygen tension was increased to normal levels by increasing the maternal inspired oxygen fraction and glucose was infused into FGR fetuses (FGR-OG). FGR-OG fetuses were compared with maternal air insufflated, saline-infused fetuses (FGR-AS) and control fetuses. Prior to treatment, FGR fetuses were hypoxemic and hypoglycemic and had reduced glucose-stimulated insulin secretion (GSIS). During treatment, oxygen, glucose, and insulin concentrations increased, and norepinephrine concentrations decreased in FGR-OG fetuses, whereas FGR-AS fetuses were unaffected. On treatment day 4, glucose fluxes were measured with euglycemic and hyperinsulinemic-euglycemic clamps. During both clamps, rates of glucose utilization and production were greater in FGR-AS than FGR-OG fetuses, while glucose fluxes in FGR-OG fetuses were not different than control rates. After 5 days of treatment, GSIS increased in FGR-OG fetuses to control levels and their ex vivo islet GSIS was greater than FGR-AS islets. Despite normalization in fetal characteristics, GSIS, and glucose fluxes, FGR-OG and FGR-AS fetuses weighed less than controls. These findings show that sustained, simultaneous correction of oxygen and glucose normalized GSIS and whole-body glucose fluxes in PI-FGR fetuses after the onset of FGR.<\/jats:p>","DOI":"10.1210\/endocr\/bqac053","type":"journal-article","created":{"date-parts":[[2022,4,21]],"date-time":"2022-04-21T17:11:27Z","timestamp":1650561087000},"source":"Crossref","is-referenced-by-count":14,"title":["Prenatal Oxygen and Glucose Therapy Normalizes Insulin Secretion and Action in Growth-Restricted Fetal Sheep"],"prefix":"10.1210","volume":"163","author":[{"given":"Leticia E","family":"Camacho","sequence":"first","affiliation":[{"name":"School of Animal and Comparative Biomedical Sciences, University of Arizona , Tucson, Arizona 85719 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melissa A","family":"Davis","sequence":"additional","affiliation":[{"name":"School of Animal and Comparative Biomedical Sciences, University of Arizona , Tucson, Arizona 85719 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amy C","family":"Kelly","sequence":"additional","affiliation":[{"name":"School of Animal and Comparative Biomedical Sciences, University of Arizona , Tucson, Arizona 85719 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nathan R","family":"Steffens","sequence":"additional","affiliation":[{"name":"School of Animal and Comparative Biomedical Sciences, University of Arizona , Tucson, Arizona 85719 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miranda J","family":"Anderson","sequence":"additional","affiliation":[{"name":"School of Animal and Comparative Biomedical Sciences, University of Arizona , Tucson, Arizona 85719 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5851-0439","authenticated-orcid":false,"given":"Sean W","family":"Limesand","sequence":"additional","affiliation":[{"name":"School of Animal and Comparative 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