{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T01:07:17Z","timestamp":1792026437032,"version":"4.4.0"},"reference-count":38,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2025,6,25]],"date-time":"2025-06-25T00:00:00Z","timestamp":1750809600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["obgyn.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acta Obstet Gynecol Scand"],"published-print":{"date-parts":[[2025,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Introduction<\/jats:title><jats:p>Human placental lactogen (hPL) is a placental hormone which, according to preclinical research, appears to have key metabolic roles in pregnancy. We aimed to examine pregnancy hPL levels in relation to maternal metabolic parameters and fetal outcomes within an ethnically diverse cohort at high metabolic risk. Design was an observational cohort study, nested within a randomized controlled trial.<\/jats:p><\/jats:sec><jats:sec><jats:title>Material and Methods<\/jats:title><jats:p>Pregnant women (<jats:italic>n<\/jats:italic>\u2009=\u2009130), recruited for high metabolic risk, underwent measurement of hPL, plus clinical and metabolic parameters, in early pregnancy (15.8\u2009\u00b1\u20092.5\u2009weeks of gestation). Univariable and multivariable simple linear regression models were used to examine relationships between early pregnancy hPL and key maternal anthropometric and biochemical variables. Fifty\u2010four women progressed to serial measurement of hPL and metabolic parameters across pregnancy. Univariable and multivariable mixed effects regression models were used to explore relationships between hPL and maternal variables across pregnancy, with repeated measures adjusted for using random effects.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In early pregnancy, lower hPL levels were independently associated with higher maternal fasting glucose (<jats:italic>\u03b2<\/jats:italic>\u2009=\u2009\u22121.03, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.01). Early pregnancy hPL was not significantly related to maternal obesity, gestational diabetes mellitus (GDM), or polycystic ovary syndrome status. In women with GDM, sampled serially across pregnancy, maternal hPL and leptin levels were inversely associated (adjusted <jats:italic>\u03b2<\/jats:italic>\u2009=\u2009\u22120.098, <jats:italic>p<\/jats:italic>\u2009\u2264\u20090.001). There was a significant relationship between higher late pregnancy hPL and increased infant birthweight in the serially sampled GDM cohort, both before (<jats:italic>\u03b2<\/jats:italic>\u2009=\u200950.81, <jats:italic>p<\/jats:italic>\u2009=\u20090.01) and after (<jats:italic>\u03b2<\/jats:italic>\u2009=\u200941.78, <jats:italic>p<\/jats:italic>\u2009=\u20090.02) adjustment for gestational age at birth.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Maternal hPL may play a role in maternal metabolic adaptation to pregnancy, particularly in relation to glucose and leptin dynamics. hPL in late pregnancy is positively associated with infant birthweight in women with GDM. Future studies of hPL in well\u2010defined contemporary populations are warranted, both to understand mechanistic interactions in pregnancy and potentially as a biomarker for infant birthweight.<\/jats:p><\/jats:sec>","DOI":"10.1111\/aogs.70000","type":"journal-article","created":{"date-parts":[[2025,6,25]],"date-time":"2025-06-25T08:14:31Z","timestamp":1750839271000},"page":"1694-1704","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Metabolic associations of human placental lactogen in pregnancies at high metabolic risk: An observational cohort study"],"prefix":"10.1111","volume":"104","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1492-483X","authenticated-orcid":false,"given":"Kate","family":"Rassie","sequence":"first","affiliation":[{"name":"Monash Centre for Health Research and Implementation (MCHRI), Faculty of Medicine, Nursing and Health Sciences, Monash University  Melbourne Victoria Australia"},{"name":"Department of Diabetes Monash Health  Melbourne Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9970-622X","authenticated-orcid":false,"given":"Simon","family":"Alesi","sequence":"additional","affiliation":[{"name":"Monash Centre for Health Research and Implementation (MCHRI), Faculty of Medicine, Nursing and Health Sciences, Monash University  Melbourne Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adriana C. 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