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瘦素:在灵长类动物妊娠中的作用与调节

Leptin: roles and regulation in primate pregnancy.

作者信息

Henson Michael C, Castracane V Daniel

机构信息

Department of Obstetrics and Gynecology, and the Tulane National Primate Research Center, Tulane University Health Sciences Center, New Orleans, Louisiana 70112-2699, USA.

出版信息

Semin Reprod Med. 2002 May;20(2):113-22. doi: 10.1055/s-2002-32502.

Abstract

Leptin, a hormone produced by adipose tissue and the placenta, is enhanced in the maternal circulation throughout pregnancy in both the human and the baboon ( Papio sp.), a proven nonhuman primate model for the study of human pregnancy. The presence of both leptin and its receptor in the fetus implies a role for the polypeptide as a regulator of in utero development, although localization in the placental trophoblast may relate to autocrine and/or paracrine regulatory functions in this important endocrine tissue. Although regulatory mechanisms remain incompletely defined, it has been suggested that cross talk occurs between the fetus, placenta, and maternal adipose stores. Placental estrogen, which is present in increasing concentrations with advancing gestation, is suggested to influence leptin synthesis in a tissue- and cell type-specific fashion. In this capacity, cellular hypoxia, diabetes, and preeclampsia are conditions that appear to be intimately linked to leptin dynamics. A better understanding of regulatory mechanisms will have direct clinical significance, as leptin has been proposed to impact on those causes of human perinatal morbidity and mortality that are associated with anomalies of fetal maturity and development, general conceptus growth, trophoblast endocrinology, and placental sufficiency.

摘要

瘦素是一种由脂肪组织和胎盘产生的激素,在人类和狒狒(狒狒属)整个孕期的母体循环中都会增加,狒狒是一种已被证实的用于研究人类妊娠的非人类灵长类动物模型。胎儿体内同时存在瘦素及其受体,这意味着该多肽在子宫内发育中具有调节作用,尽管其在胎盘滋养层中的定位可能与这个重要内分泌组织中的自分泌和/或旁分泌调节功能有关。尽管调节机制仍未完全明确,但有人提出胎儿、胎盘和母体脂肪储存之间会发生相互作用。随着妊娠进展,胎盘雌激素浓度不断升高,有人认为它会以组织和细胞类型特异性的方式影响瘦素的合成。在这种情况下,细胞缺氧、糖尿病和先兆子痫似乎与瘦素动态密切相关。更好地理解调节机制将具有直接的临床意义,因为有人提出瘦素会影响那些与胎儿成熟和发育异常、总体胚胎生长、滋养层内分泌学以及胎盘功能不全相关的人类围产期发病和死亡原因。

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