妊娠不同时期脂肪细胞因子的动态变化与胰岛素抵抗的关系

目的探讨妊娠不同时期脂肪细胞因子的动态变化及其与孕妇胰岛素抵抗的关系。方法选择2004年10月—2005年10月在我院门诊行产前检查的正常孕妇67例,其中妊娠早期18例(妊娠早期组),妊娠中期19例(妊娠中期组),妊娠晚期30例(妊娠晚期组);另选同期正常非孕妇女46例为对照组。采用酶联免疫吸附试验检测各组妇女血清中可溶性肿瘤坏死因子α受体(sTNFR)-Ⅰ、Ⅱ水平;采用放射免疫法测定各组妇女血清中瘦素、脂联素水平;采用免疫组化链霉菌抗生物素蛋白-过氧化物酶连接(SP)法检测妊娠晚期组妇女胎盘及脂肪组织中sTNFR定位与阳性表达。结果(1)妊娠早、中、晚期组及对照组妇女血清中sTNFR-Ⅰ水平分别为(799±173)、(1003±241)、(1278±306)及(729±167)ng/L,妊娠中、晚期组明显高于对照组,分别比较,差异有统计学意义(P<0·001)。(2)妊娠早、中、晚期组及对照组妇女血清中sTNFR-Ⅱ水平分别为(1383±305)、(1772±293)、(1933±498)及(1002±221)ng/L,妊娠早、中、晚期组明显高于对照组,分别比较,差异均有统计学意义(P<0·001)。并随孕期的增加,sTNFR-Ⅱ水平不断升高。(3)妊娠早、中、晚期组及对照组妇女血清中瘦素水平分别为(65±37)、(70±40)、(89±57)及(61±37)μg/L,妊娠晚期组明显高于对照组,两组比较,差异有统计学意义(P<0·05)。(4)妊娠早、中、晚期组及对照组妇女血清中脂联素水平分别为(13±6)、(9±5)、(10±4)及(14±7)mg/L,妊娠中、晚期组明显低于对照组,分别比较,差异有统计学意义(P<0·05)。(5)妊娠晚期组妇女胎盘及脂肪组织中sTNFR-Ⅰ、Ⅱ均呈阳性表达,无阴性表达;sTNFR-Ⅰ阳性染色颗粒主要定位于胎盘绒毛组织中的合体滋养细胞以及细胞滋养细胞中的胞质和胞膜,sTNFR-Ⅱ阳性染色颗粒主要定位于胎盘血管内皮细胞中的胞质和胞膜。结论孕妇血清中sTNFR-Ⅰ、Ⅱ及瘦素水平随孕期的增加不断升高;而脂联素水平则随孕期的增加有所下降,上述变化可能与孕妇的胰岛素抵抗有关。

Correlation of adipocytokines and insulin resistance in normal pregnancy

OBJECTIVE: To explore the dynamic changes of adipocytokines and its correlation with insulin resistance during different stages of normal pregnancy. METHODS: Sixty-seven healthy pregnant women (18 first, 19 second and 30 third trimester) as experimental groups and 46 healthy age-matched non-pregnant women as a control group were investigated in a case-control cross-sectional study. Serum soluble tumor necrosis factor receptor (sTNFR) was determined by enzyme linked immunoadsorbent assay (ELISA). Maternal serum leptin and adiponectin were detected by radial immunodiffusion. TNF-alphaR in placenta and fat tissue was examined by streptavidin/peroxidase. RESULTS: The sTNFR-I level was higher in pregnant women than that in the control group (729 +/- 167) ng/L, being significantly higher in second (1003 +/- 241) ng/L and third trimesters (1278 +/- 306) ng/L (P < 0.001). sTNFR-II level of first, second and third trimester groups (1383 +/- 305) ng/L, (1772 +/- 293) ng/L, (1933 +/- 498) ng/L was higher than that in the control group (1002 +/- 221) ng/L (P < 0.001) and was increased with the progress of gestation. Leptin level in late trimester (89 +/- 57) microg/L was significantly higher than that in control group (61 +/- 37) microg/L (P < 0.05). Adiponectin level in second (9 +/- 5) mg/L and third trimesters (10 +/- 4) mg/L was significantly lower than that in control group (14 +/- 7) mg/L (P < 0.05). The sTNFR-I and sTNFR-II were expressed in placenta and fat tissue. CONCLUSION: The dynamic changes of adipocytokines contribute to occurrence of insulin resistance.