Ericsson Anette, Hamark Bengt, Jansson Nina, Johansson Bengt R, Powell Theresa L, Jansson Thomas
Perinatal Center, Dept. of Physiology and Pharmacology, Göteborg University, Box 432, 405 30 Göteborg, Sweden.
Am J Physiol Regul Integr Comp Physiol. 2005 Mar;288(3):R656-62. doi: 10.1152/ajpregu.00407.2004. Epub 2004 Nov 11.
Alterations in placental nutrient transfer have been implicated in fetal growth abnormalities. In pregnancies complicated by diabetes and accelerated fetal growth, upregulations of glucose transporter 1 (GLUT1) and amino acid transporter system A have been shown in the syncytiotrophoblast of term placenta. In contrast, intrauterine growth restriction is associated with a downregulation of placental system A transporters. However, underlying mechanisms of transporter regulation are poorly understood, particularly in early pregnancy. In this study, hormonal regulation of placental glucose and system A transporters was investigated. The uptake of 3-O-[methyl-(14)C]-d-glucose was studied in villous fragments isolated from first trimester (6-13 wk of gestation) and term human placenta. Villous fragments were incubated in buffer containing insulin, leptin, cortisol, growth hormone (GH), prolactin, IGF-I, or under hypo/hyperglycemic conditions for 1 h. Subsequently, 3-O-[methyl-(14)C]-D-glucose uptake was measured with and without phloretin for 70 s in first trimester tissue and 20 s in term tissue. Methylaminoisobutyric uptake was measured with and without Na+ for 20 min. Glucose uptake was unaltered by hormones or hypo/hyperglycemia. GH decreased system A activity by 31% in first trimester (P < 0.05). The uptake of glucose was 50% higher in term compared with first trimester fragments and increased markedly between 6 and 13 wk of gestation (P < 0.05). We conclude that placental glucose transporter activity is not regulated by short exposures to the hormones or glucose concentrations tested. In contrast to term placental villous fragments, system A activity was not regulated by insulin or leptin in first trimester but was downregulated by GH.
胎盘营养物质转运的改变与胎儿生长异常有关。在合并糖尿病且胎儿生长加速的妊娠中，足月胎盘的合体滋养层中已显示葡萄糖转运蛋白1（GLUT1）和氨基酸转运系统A上调。相反，宫内生长受限与胎盘系统A转运蛋白的下调有关。然而，转运蛋白调节的潜在机制尚不清楚，尤其是在妊娠早期。在本研究中，研究了胎盘葡萄糖和系统A转运蛋白的激素调节。在从妊娠早期（妊娠6 - 13周）和足月人胎盘中分离出的绒毛片段中研究了3 - O - [甲基 - （14）C] - D - 葡萄糖的摄取。绒毛片段在含有胰岛素、瘦素、皮质醇、生长激素（GH）、催乳素、IGF - I的缓冲液中或在低血糖/高血糖条件下孵育1小时。随后，在妊娠早期组织中测量70秒、足月组织中测量20秒有无根皮素时3 - O - [甲基 - （14）C] - D - 葡萄糖的摄取。在有无Na + 的情况下测量甲基氨基异丁酸摄取20分钟。葡萄糖摄取不受激素或低血糖/高血糖的影响。GH使妊娠早期系统A活性降低31%（P < 0.05）。与妊娠早期片段相比，足月时葡萄糖摄取高出50%，且在妊娠6至13周之间显著增加（P < 0.05）。我们得出结论，胎盘葡萄糖转运蛋白活性不受所测试的激素或葡萄糖浓度短时间暴露的调节。与足月胎盘绒毛片段相反，妊娠早期系统A活性不受胰岛素或瘦素调节，但受GH下调。
