Placental fatty acid transport in maternal obesity

被引:36
作者
Cetin, I. [1 ]
Parisi, F. [1 ]
Berti, C. [1 ]
Mando, C. [1 ]
Desoye, G. [2 ]
机构
[1] Univ Milan, Dept Clin Sci L Sacco, Unit Obstet & Gynecol, I-20157 Milan, Italy
[2] Med Univ Graz, Dept Obstet & Gynaecol, Graz, Austria
关键词
fatty acids; maternal obesity; placental transport; pregnancy; INTRAUTERINE GROWTH RESTRICTION; BINDING PROTEINS; LIPID-METABOLISM; NORMAL-PREGNANCY; FETAL; WOMEN; WEIGHT; PLASMA; DYSREGULATION; INFLAMMATION;
D O I
10.1017/S2040174412000414
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
Pregestational obesity is a significant risk factor for adverse pregnancy outcomes. Maternal obesity is associated with a specific proinflammatory, endocrine and metabolic phenotype that may lead to higher supply of nutrients to the feto-placental unit and to excessive fetal fat accumulation. In particular, obesity may influence placental fatty acid ( FA) transport in several ways, leading to increased diffusion driving force across the placenta, and to altered placental development, size and exchange surface area. Animal models show that maternal obesity is associated with increased expression of specific FA carriers and inflammatory signaling molecules in placental cotyledonary tissue, resulting in enhanced lipid transfer across the placenta, dislipidemia, fat accumulation and possibly altered development in fetuses. Cell culture experiments confirmed that inflammatory molecules, adipokines and FA, all significantly altered in obesity, are important regulators of placental lipid exchange. Expression studies in placentas of obese-diabetic women found a significant increase in FA binding protein-4 expression and in cellular triglyceride content, resulting in increased triglyceride cord blood concentrations. The expression and activity of carriers involved in placental lipid transport are influenced by the endocrine, inflammatory and metabolic milieu of obesity, and further studies are needed to elucidate the strong association between maternal obesity and fetal overgrowth.
引用
收藏
页码:409 / 414
页数:6
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