Document Detail


Leptin in pregnancy: an update.
MedLine Citation:
PMID:  16267210     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Leptin influences satiety, adiposity, and metabolism and is associated with mechanisms regulating puberty onset, fertility, and pregnancy in various species. Maternal hyperleptinemia is a hallmark of mammalian pregnancy, although both the roles of leptin and the mechanisms regulating its synthesis appear to be taxa specific. In pregnant humans and nonhuman primates, leptin is produced by both maternal and fetal adipose tissues, as well as by the placental trophoblast. Specific receptors in the uterine endometrium, trophoblast, and fetus facilitate direct effects of the polypeptide on implantation, placental endocrine function, and conceptus development. A soluble isoform of the receptor may be responsible for inducing maternal leptin resistance during pregnancy and/or may facilitate the transplacental passage of leptin for the purpose of directly regulating fetal development. The steroid hormones are linked to the regulation of leptin and the leptin receptor and probably interact with other pregnancy-specific, serum-borne factors to regulate leptin dynamics during pregnancy. In addition to its effects on normal conceptus development, leptin is linked to mechanisms affecting a diverse array of pregnancy-specific pathologies that include preeclampsia, gestational diabetes, and intrauterine growth restriction. Association with these anomalies and with mechanisms pointing to a fetal origin for a range of conditions affecting the individual's health in adult life, such as obesity, diabetes mellitus, and cardiovascular disease, reiterate the need for continued research dedicated to elucidating leptin's roles and regulation throughout gestation.
Authors:
Michael C Henson; V Daniel Castracane
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2005-11-02
Journal Detail:
Title:  Biology of reproduction     Volume:  74     ISSN:  0006-3363     ISO Abbreviation:  Biol. Reprod.     Publication Date:  2006 Feb 
Date Detail:
Created Date:  2006-01-26     Completed Date:  2006-04-10     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0207224     Medline TA:  Biol Reprod     Country:  United States    
Other Details:
Languages:  eng     Pagination:  218-29     Citation Subset:  IM    
Affiliation:
Department of Obstetrics and Gynecology, Tulane University Health Sciences Center, New Orleans, Louisiana 70112-2699, USA. michaelchenson@bellsouth.net
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MeSH Terms
Descriptor/Qualifier:
Animals
Female
Humans
Leptin / physiology*
Pregnancy / metabolism*
Pregnancy Complications / metabolism
Receptors, Cell Surface / metabolism*
Receptors, Leptin
Steroids / metabolism
Grant Support
ID/Acronym/Agency:
P51 RR00164/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Leptin; 0/Receptors, Cell Surface; 0/Receptors, Leptin; 0/Steroids; 0/leptin receptor, human

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