Cited by 488Growth Hormone and Insulin-like Growth FactorsPregnancy and preeclampsia studiesGestational Diabetes Research and Management

Placental hormones and the control of maternal metabolism and fetal growth

Newbern, Dorothee, Freemark, Michael·2011·Current Opinion in Endocrinology, Diabetes & Obesity

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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Crossref · 10.1097/med.0b013e32834c800d

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69 of 69 references verified0 citation errors · 0 not checkable

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  • 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.

    “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]

  • Progesterone and human placental lactogen stimulate maternal appetite during early pregnancy, enabling deposition of maternal adipose energy reserves that can be used later in pregnancy and during lactation.

    “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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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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