Journal
CURRENT OPINION IN ENDOCRINOLOGY DIABETES AND OBESITY
Volume 18, Issue 6, Pages 409-416Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MED.0b013e32834c800d
Keywords
growth hormone; insulin; insulin-like growth factor; placental lactogen; prolactin
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Funding
- Endocrine Fellows Foundation
- NIH
- NICHD
- American Diabetes Association
- Duke Children's Medical Network
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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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