The DOI matches its Crossref record; 69 of the 70 references it cites were found in a registry or an index.
Placental hormones and the control of maternal metabolism and fetal growth
Abstract
PURPOSE OF REVIEW: To examine the roles of the placental and pituitary hormones in the control of maternal metabolism and fetal growth. RECENT FINDINGS: In addition to promoting growth of maternal tissues, placental growth hormone (GH-V) induces maternal insulin resistance and thereby facilitates the mobilization of maternal nutrients for fetal growth. Human placental lactogen (hPL) and prolactin increase maternal food intake by induction of central leptin resistance and promote maternal beta-cell expansion and insulin production to defend against the development of gestational diabetes mellitus. The effects of the lactogens are mediated by diverse signaling pathways and are potentiated by glucose. Pathologic conditions of pregnancy are associated with dysregulation of GH-V and hPL gene expression. SUMMARY: The somatogenic and lactogenic hormones of the placenta and maternal pituitary gland integrate the metabolic adaptations of pregnancy with the demands of fetal and neonatal development. Dysregulation of placental growth hormone and/or placental lactogen in pathologic conditions of pregnancy may adversely impact fetal growth and postnatal metabolic function.
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“This is perhaps not surprising given that a proportion of the nutrients that support fetal growth, particularly in late pregnancy, come from turnover of maternal fat reserves that are built up in early pregnancy (414).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [414]
In the citing paper
“Progesterone also stimulates maternal appetite during early pregnancy, as does human placental lactogen (hPL), enabling the deposition of maternal adipose energy reserves that can be utilized later in pregnancy and during lactation (414).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [414]
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“…that occur in the metabolic syndrome, including weight gain, elevated fasting bloodglucose levels, insulin resistance, glucose intolerance, lowgrade inflammation, and changes in metabolic hormone levels (Fuglsang, 2008; Newbern and Freemark, 2011; Emanuela et al., 2012; Kumar and Magon, 2012).”
Background
Metadata
- Authors
- Newbern, D., & Freemark, M.
- Affiliations
- Duke University (US)
- Corresponding author
- Newbern, Dorothee
- Venue
- Current Opinion in Endocrinology, Diabetes & Obesity
- Published
- 2011-12
- Volume
- 18
- Issue
- 6
- Pages
- 409-416
- ISSN
- 1752-296X (ISSN-L)
- OpenAlex
- W2160934677
- Cited by
- 487
- References
- 70
- Citations by year
- 2026: 15 · 2025: 27 · 2024: 43 · 2023: 24 · 2022: 46 · 2021: 49 · 2020: 54 · 2019: 40 · 2018: 35 · 2017: 34 · 2016: 33 · 2015: 27 · 2014: 28 · 2013: 19 · 2012: 12
- FWCI
- 2.63
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Endocrinology Diabetes and Obesity (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Endocrine Fellows Foundation
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Keywords
- placental hormones, maternal metabolism, fetal growth, placental growth hormone, human placental lactogen, prolactin, leptin resistance, maternal insulin resistance, gestational diabetes mellitus, beta-cell expansion, glucose signaling, pregnancy complications, pituitary hormones
- MeSH terms
- Female, Fetus, Glucocorticoids, Humans, Insulin, Maternal-Fetal Exchange, Pituitary Gland, Placenta, Placental Hormones, Pregnancy, Leptin, Fetal Development, Adipokines
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