Laboratoire de Physiologie Materno-Fœtale, Département des Sciences Biologiques, Université du Québec à Montréal, Montréal, Québec, Canada.
Biol Reprod. 2012 Jul 19;87(1):14, 1-11. doi: 10.1095/biolreprod.111.098095. Print 2012 Jul.
Knowledge of the consequences of maternal obesity in human placental fatty acids (FA) transport and metabolism is limited. Animal studies suggest that placental uptake of maternal FA is altered by maternal overnutrition. We hypothesized that high maternal body mass index (BMI) affects human placental FA transport by modifying expression of key transporters. Full-term placentas were obtained by vaginal delivery from normal weight (BMI, 18.5-24.9 kg/m(2)) and obese (BMI > 30 kg/m(2)) women. Blood samples were collected from the mother at each trimester and from cord blood at delivery. mRNA and protein expression levels were evaluated with real-time RT-PCR and Western blotting. Lipoprotein lipase (LPL) activity was evaluated using enzyme fluorescence. In vitro linoleic acid transport was studied with isolated trophoblasts. Our results demonstrated that maternal obesity is associated with increased placental weight, decreased gestational age, decreased maternal high-density lipoprotein (HDL) levels during the first and third trimesters, increased maternal triglyceride levels during the second and third trimesters, and increased maternal T3 levels during all trimesters, and decreased maternal cholesterol (CHOL) and low-density lipoprotein (LDL) levels during the third trimester; and increased newborn CHOL, LDL, apolipoprotein B100, and T3 levels. Increases in placental CD36 mRNA and protein expression levels, decreased SLC27A4 and FABP1 mRNA and protein and FABP3 protein expression, and increased LPL activity and decreased villus cytotrophoblast linoleic acid transport were also observed. No changes were seen in expression of PPARA, PPARD, or PPARG mRNA and protein. Overall this study demonstrated that maternal obesity impacts placental FA uptake without affecting fetal growth. These changes, however, could modify the fetus metabolism and its predisposition to develop diseases later in life.
母体肥胖对人胎盘脂肪酸（FA）转运和代谢的影响知之甚少。动物研究表明，母体营养过剩会改变胎盘对母体 FA 的摄取。我们假设高母体体重指数（BMI）通过改变关键转运体的表达来影响人胎盘 FA 转运。通过阴道分娩获得正常体重（BMI，18.5-24.9kg/m2）和肥胖（BMI>30kg/m2）妇女的足月胎盘。在每个孕期从母亲和分娩时从脐血采集血样。用实时 RT-PCR 和 Western 印迹法评估 mRNA 和蛋白表达水平。用酶荧光法评估脂蛋白脂肪酶（LPL）活性。用分离的滋养层细胞研究亚油酸的体外转运。我们的结果表明，母体肥胖与胎盘重量增加、胎龄减少、第一和第三孕期母体高密度脂蛋白（HDL）水平降低、第二和第三孕期母体甘油三酯水平升高、所有孕期母体 T3 水平升高以及第三孕期母体胆固醇（CHOL）和低密度脂蛋白（LDL）水平降低有关；新生儿 CHOL、LDL、载脂蛋白 B100 和 T3 水平升高。胎盘 CD36mRNA 和蛋白表达水平升高，SLC27A4 和 FABP1mRNA 和蛋白表达降低，FABP3 蛋白表达降低，LPL 活性增加，绒毛细胞滋养层亚油酸转运减少。PPARA、PPARD 和 PPARGmRNA 和蛋白表达无变化。总的来说，这项研究表明，母体肥胖会影响胎盘 FA 的摄取，而不影响胎儿的生长。然而，这些变化可能会改变胎儿的新陈代谢及其在以后的生活中易患疾病的倾向。
