{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zamudio S"],"funding":["NICHD NIH HHS","FIC NIH HHS"],"pagination":["e8551"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2797307"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["5(1)"],"pubmed_abstract":["<h4>Background</h4>The most well known reproductive consequence of residence at high altitude (HA >2700 m) is reduction in fetal growth. Reduced fetoplacental oxygenation is an underlying cause of pregnancy pathologies, including intrauterine growth restriction and preeclampsia, which are more common at HA. Therefore, altitude is a natural experimental model to study the etiology of pregnancy pathophysiologies. We have shown that the proximate cause of decreased fetal growth is not reduced oxygen availability, delivery, or consumption. We therefore asked whether glucose, the primary substrate for fetal growth, might be decreased and/or whether altered fetoplacental glucose metabolism might account for reduced fetal growth at HA.<h4>Methods</h4>Doppler and ultrasound were used to measure ma"],"journal":["PloS one"],"pubmed_title":["Hypoglycemia and the origin of hypoxia-induced reduction in human fetal growth."],"pmcid":["PMC2797307"],"funding_grant_id":["HD042737","R03 TW007444","HD046982","TW007444","R01 HD042737","R01 HD046982"],"pubmed_authors":["Illsley NP","Balanza E","Pullockaran J","Tutino E","Fik E","Echalar L","Torricos T","Oyala M","Belliappa S","Martin B","Zamudio S"],"additional_accession":[]},"is_claimable":false,"name":"Hypoglycemia and the origin of hypoxia-induced reduction in human fetal growth.","description":"<h4>Background</h4>The most well known reproductive consequence of residence at high altitude (HA >2700 m) is reduction in fetal growth. Reduced fetoplacental oxygenation is an underlying cause of pregnancy pathologies, including intrauterine growth restriction and preeclampsia, which are more common at HA. Therefore, altitude is a natural experimental model to study the etiology of pregnancy pathophysiologies. We have shown that the proximate cause of decreased fetal growth is not reduced oxygen availability, delivery, or consumption. We therefore asked whether glucose, the primary substrate for fetal growth, might be decreased and/or whether altered fetoplacental glucose metabolism might account for reduced fetal growth at HA.<h4>Methods</h4>Doppler and ultrasound were used to measure ma","dates":{"release":"2010-01-01T00:00:00Z","publication":"2010 Jan","modification":"2026-07-15T07:37:13.588Z","creation":"2026-07-01T03:07:46.904Z"},"accession":"S-EPMC2797307","cross_references":{"pubmed":["20049329"],"doi":["10.1371/journal.pone.0008551"]}}