4.5 Article

Cytokine profile, metabolic syndrome and cardiovascular disease risk in women with late-onset gestational diabetes mellitus

期刊

CYTOKINE
卷 58, 期 1, 页码 14-19

出版社

ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.cyto.2011.12.004

关键词

Gestational diabetes mellitus; Cytokine; Cardiovascular disease risk; Pregnancy

资金

  1. Andalusia Department of Health [CTS-368]

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Inflammation is an important component of the metabolic syndrome (MetS) which could be the link between the metabolic and the cardiovascular consequences of this condition. Gestational diabetes mellitus (GDM) has been recognized as a significant risk factor for MetS and an inflammation component has been described in this disease. The aim of the study was to evaluate the relationships between cytokine concentrations, components of MetS and cardiovascular risk markers in women with late-onset GDM. Women (n = 63) with late-onset GDM and 63 controls were enrolled. Clinical variables, and obstetrics and perinatal outcomes were recorded. Relationships between cytokines (TNF-alpha, leptin, IL6, adiponectin) and endothelial injury markers (VCAM, ICAM and selectine) were analyzed. Control vs. patient data indicated: pre-gestational body mass index (BMI) 23.46 +/- 3.73 vs. 26.97 +/- 5.07 kg/m(2) (p = 0.001); TNF-alpha 2.2 +/- 0.8 vs. 3.1 +/- 1.5 pg/mL (p = 0.002); leptin 18714.78 +/- 8859.08 vs. 27365.79 +/- 16209.67 pg/mL (p = 0.001); adiponectin 162.42 +/- 34.19 vs. 141.54 +/- 41.33 ng/mL (p = 0.04). Multivariate analyses showed that adiponectin had a protective effect (OR = 0.9; p = 0.02) and BMI carried a significant risk (OR = 8.4; p = 0.01) for GDM. No differences were found in endothelial injury markers. In conclusion, the cytokine profile in women with late-onset GDM is characterized by high concentrations of TNF-alpha and leptin and low adiponectin. This profile is related, in large extent, to an increased pregravid BMI which, potentially, may be linked to the future development of both metabolic and cardiovascular disease. (C) 2011 Elsevier Ltd. All rights reserved.

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