Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2011 Dec;18(6):409-16.
doi: 10.1097/MED.0b013e32834c800d.

Placental hormones and the control of maternal metabolism and fetal growth

Affiliations
Review

Placental hormones and the control of maternal metabolism and fetal growth

Dorothee Newbern et al. Curr Opin Endocrinol Diabetes Obes. 2011 Dec.

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.

PubMed Disclaimer

Publication types

LinkOut - more resources