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子痫前期患者胎盘瘦素对血清瘦素水平及缺氧对胎盘瘦素合成的影响 被引量:1

Contribution of placental leptin to the serum levels in preeclampsia and effect of hypoxia on synthesis of placental leptin
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摘要 目的:探讨妊娠期高血压疾病子痫前期患者胎盘与血清瘦素水平的关系及缺氧对胎盘绒毛合成瘦素的影响.方法:应用RIA法测定孕妇肘前静脉及胎盘附着部位子宫静脉血血清瘦素水平,其中妊娠期高血压疾病子痫前期患者(研究组)15例,正常妊娠妇女(对照组)20例;并在缺氧(20mL/LO2)及常氧(210mL/LO2)环境下培养8例正常足月胎盘绒毛,通过RIA法检测胎盘绒毛培养液中瘦素的含量.结果:研究组外周血瘦素水平为23.29±12.87μg/L,对照组为13.87±5.57μg/L,两组比较差异有统计学意义(P<0.05);研究组子宫静脉血瘦素水平为16.44±8.62μg/L,对照组为11.21±4.20μg/L,两组比较有统计学意义(P<0.05).研究组和对照组外周血瘦素水平均高于子宫静脉血(P<0.05).在缺氧条件下胎盘绒毛培养上清中瘦素的含量高于常氧条件下(P<0.05).结论:妊娠期高血压疾病患者胎盘及血清中瘦素的水平升高,可能与妊娠期高血压疾病发病有关,而且胎盘缺氧可能是胎盘瘦素合成增加的重要因素之一.胎盘只是正常妊娠孕妇及妊娠期高血压疾病患者血中瘦素增加的来源之一. AIM: [JP3]To investigate the contribution of placental leptin to the serum levels and the effect of hypoxia on synthesis of placental leptin. METHODS: Fifteen preeclamptic women and 20 normotensive pregnant women were recruited in present study. Leptin concentrations in peripheral venous blood samples and uterine venous blood samples were measured by radioimmunoassay. Eight cases of normal human term placental villi were cultured either in normaxia (210 mL/L O2) or in hypoxia (20 mL/L O2) followed by determining leptin in the culture medium by radioimmunoassay. RESULTS: Leptin concentrations were significantly higher in preeclamptic women than in normotensive pregnant women, both in the peripheral vein (23.29±12.87 μg/L vs 13.87±5.57 μg/L, P<0.05) and uterine vein (16.44±8.62 μg/L vs 11.21±4.20 μg/L, P<0.05). Leptin concentration were significantly higher in the peripheral vein than in uterine vein, both in the preeclamptic (P<0.05) and in normotensive pregnant women (P<0.05). Concentrations of leptin in the culture medium were significantly increased in hypoxia than in normoxia (P<0.05). CONCLUSION: The pathogenesis of preeclampsia may be associated with an increase of maternal serum leptin and placenta leptin, and hypoxia in placenta may be an important factor that results in preeclamptic placenta to produce more leptin. Placenta is not the principal source of the serum leptin in the preeclamptic women or normotensive pregnant women.
出处 《第四军医大学学报》 北大核心 2005年第12期1083-1085,共3页 Journal of the Fourth Military Medical University
基金 国家自然科学基金(30070787)
关键词 先兆子痫 瘦素 缺氧 pre-eclampsia leptin hypoxia
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参考文献12

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同被引文献14

  • 1隋满姝,刘素雁,阮颖新,杜玄一,刘晓刚.瘦素受体基因多态性及瘦素水平对应用糖皮质激素患者骨量的影响[J].中华肾脏病杂志,2006,22(5):308-310. 被引量:4
  • 2Adali E, Yildizhan R, Kolusari A, et al. Increased visfatin and leptin in pregnancies complicated lay pre-eclampsia. J Matern Fetal Neonatal Med, 2009,22 : 873-879.
  • 3Laivuori H,Gallaher MJ,Collura L,et al. Relationships between maternal plasma leptin, placental leptin mRNA and protein in normal pregnancy, pre-eclampsia and intrauterine growth restriction without pre-eclampsia. Mol Hum Reprod, 2006,12: 551-556.
  • 4Linnemann K, Malek A, Schneider H, et al. Physiological and pathological regulation of feto/placento/mat ernal leptin expression. Biolchem Soc Trans, 2001,29 : 86-90.
  • 5Hendler I,Blackwell SC, Mehta SH, et al. The levels of leptin, adiponeetin, and resistin in normal weight, overweight, and obese pregnant women with and without preeclampsia. Am J Obstect Gynecol,2005,193:979-983.
  • 6Rigo J, Szendei G, Rosta K, et al. Leptin receptor gene polymorphisms in severely pre-eclamptic women. Gynecol Endocrinol, 2006,22 : 521-525.
  • 7Matsuoka N,Ogawa Y, Hosoda K, et al. Human leptin receptor gene in obese Japanese subjects., evidence against either obesitycausing mutations or association of sequence variants with obesity. Diabetologia, 1997,40 :1204-1210.
  • 8Mise H,Yura S,Itoh H,et al. The relationship between matenal plasma leptin levels and fetal growth restriction. Endocr J,2007, 54:945-951.
  • 9Mise H, Sagawa N, Matsumoto T, et al. Augmented placental production of leptin in preeclampsia: possible involvement of placental hypoxia. J Clin Endocrinol Metab, 1998,83 : 3225-3229.
  • 10Atamer Y,Erden AC, Demir B, et al. The relationship between plasma levels of leptin and androgen in healthy and preeclamptic pregnant women. Acta Obstect Gynecol Scand, 2004, 83: 425- 430.

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