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Reduced circulating levels of TWEAK are associated with Gestational Diabetes Mellitus

Background To evaluate the inflammatory axis mediated by tumour necrosis factor‐like weak inducer of apoptosis (TWEAK) and its scavenger receptor CD163 during pregnancy and their influence on insulin sensitivity in normal pregnancy and in gestational diabetes mellitus (GDM). Materials and methods On...

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Published in:European journal of clinical investigation 2015-01, Vol.45 (1), p.27-35
Main Authors: Simón-Muela, Inmaculada, Llauradó, Gemma, Chacón, Matilde Rodriguez, Olona, Montserrat, Näf, Silvia, Maymó-Masip, Elsa, Gil, Pilar, de la Flor, Miriam, Gonzalez Clemente, Jose Miguel, Vendrell, Joan, Megía, Ana
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Language:English
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Summary:Background To evaluate the inflammatory axis mediated by tumour necrosis factor‐like weak inducer of apoptosis (TWEAK) and its scavenger receptor CD163 during pregnancy and their influence on insulin sensitivity in normal pregnancy and in gestational diabetes mellitus (GDM). Materials and methods One hundred and thirty seven women with one singleton pregnancy, 71 with normal glucose tolerance (NGT) and 66 with GDM were studied. Glucose metabolism was assessed by oral glucose tolerance test. Serum concentrations of soluble TWEAK (sTWEAK) and CD163 (sCD163) and insulin resistance (HOMA‐IR index) were determined in maternal blood drawn at recruitment, in the early third trimester. Offspring weight and height were assessed at birth. Results Women with GDM had lower circulating sTWEAK concentrations than control NGT group (237·8 (192·1–301·0) pg/mL vs. 277·2 (206·4–355·7) pg/mL; P = 0·013). sTWEAK was negatively associated with the presence of GDM (r = −0·212; P = 0·013), HOMA‐IR index (r = −0·197; P = 0·021) and ponderal index of the newborn (r = −0·196; P = 0·025), but positively with HDL cholesterol (r = 0·283; P = 0·001). In multiple regression analysis, sTWEAK concentration emerged as one of the main predictors of insulin resistance, along with BMI, triglycerides and low concentrations of HDL cholesterol (R2 = 0·486; P 
ISSN:0014-2972
1365-2362
DOI:10.1111/eci.12375