Leptin in pregnancy

被引:174
作者
Henson, MC
Castracane, VD
机构
[1] Tulane Univ, Hlth Sci Ctr, Dept Obstet & Gynecol SL11, New Orleans, LA 70112 USA
[2] Tulane Univ, Hlth Sci Ctr, Dept Cellular & Struct Biol, New Orleans, LA 70112 USA
[3] Tulane Reg Primate Res Ctr, Covington, LA 70433 USA
[4] Texas Tech Univ, Hlth Sci Ctr, Dept Obstet & Gynecol, Amarillo, TX 79106 USA
[5] Texas Tech Univ, Hlth Sci Ctr, Womens Hlth Res Inst Amarillo, Amarillo, TX 79106 USA
[6] Tulane Univ, Hlth Sci Ctr, Dept Physiol, New Orleans, LA 70112 USA
关键词
conceptus; gene regulation; hormone action; leptin; leptin receptor; placenta; pregnancy; syncytiotrophoblast;
D O I
10.1095/biolreprod63.5.1219
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Leptin is a polypeptide hormone that aids in the regulation of body weight and energy homeostasis and is linked to a variety of reproductive processes in both animals and humans. Thus, leptin may help regulate ovarian development and steroidogenesis and serve as either a primary signal initiating puberty or as a permissive regulator of sexual maturation. Perhaps significantly, peripheral leptin concentrations, adjusted for adiposity, are dramatically higher in females than in males throughout life. During primate pregnancy, maternal levels that arise from adipose stores and perhaps the placenta increase with advancing gestational age. Proposed physiological roles for leptin in pregnancy include the regulation of conceptus growth and development, fetal/placental angiogenesis, embryonic hematopoiesis, and hormone biosynthesis within the maternal-fetoplacental unit The specific localization of both leptin and its receptor in the syncytiotrophoblast implies autocrine and/or paracrine relationships in this endocrinologically active tissue. Interactions of leptin with mechanisms regulating pre-eclampsia and maternal diabetes have also been suggested. Collectively, therefore, reports suggest that a better understanding of the regulation of leptin and its role(s) throughout gestation may eventually impact those causes of human perinatal morbidity and mortality that are exacerbated by intrauterine growth retardation, macrosomia, placental insufficiency, or prematurity.
引用
收藏
页码:1219 / 1228
页数:10
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