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Serum levels of leptin, adiponectin and resistin in relation to clinical characteristics in normal pregnancy and preeclampsia.
BACKGROUND: Alterations in serum adipokines in preeclampsia remain vague. We investigated the roles of leptin, adiponectin and resistin and their relationships with clinical characteristics in normotensive and preeclamptic patients.
METHODS: A case-control study was carried out in a cohort of 74 preeclampsia(PE) and 79 healthy pregnant women. Serum levels of leptin, adiponectin and resistin were measured by enzyme-linked immunosorbent assay.
RESULTS: The mean body mass index(BMI), the serum leptin and resistin levels were significantly higher in the PE group than in the control group (p<0.001). The resistin/creatinine ratio was also higher in the PE group than in the control group (p=0.018). No significant difference was observed in the serum adiponectin level between both groups. Serum leptin levels were positively correlated with BMI (r=0.301, p<0.001) and negatively correlated with newborn birth weight (r=-0.435, p<0.001). Serum resistin levels were also negatively correlated with birth weight (r=-0.229, p=0.005) but were unrelated to BMI. Logistic regression showed that BMI≥28 and serum leptin levels were independent factors of PE. Leptin was a potential mediator between BMI and PE (p<0.001), and the mediating effect accounted for 22.54% of the total effect.
CONCLUSIONS: Leptin, resistin, and obesity play important roles in the onset of PE. Leptin and resistin may have some impacts on the fetal growth and development.
METHODS: A case-control study was carried out in a cohort of 74 preeclampsia(PE) and 79 healthy pregnant women. Serum levels of leptin, adiponectin and resistin were measured by enzyme-linked immunosorbent assay.
RESULTS: The mean body mass index(BMI), the serum leptin and resistin levels were significantly higher in the PE group than in the control group (p<0.001). The resistin/creatinine ratio was also higher in the PE group than in the control group (p=0.018). No significant difference was observed in the serum adiponectin level between both groups. Serum leptin levels were positively correlated with BMI (r=0.301, p<0.001) and negatively correlated with newborn birth weight (r=-0.435, p<0.001). Serum resistin levels were also negatively correlated with birth weight (r=-0.229, p=0.005) but were unrelated to BMI. Logistic regression showed that BMI≥28 and serum leptin levels were independent factors of PE. Leptin was a potential mediator between BMI and PE (p<0.001), and the mediating effect accounted for 22.54% of the total effect.
CONCLUSIONS: Leptin, resistin, and obesity play important roles in the onset of PE. Leptin and resistin may have some impacts on the fetal growth and development.
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