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The Journal of Clinical Endocrinology & Metabolism Vol. 89, No. 10 5081-5087
Copyright © 2004 by The Endocrine Society

Mannose-Binding Lectin Gene Polymorphisms Are Associated with Gestational Diabetes Mellitus

Anna Megia, Lluis Gallart, Jose-Manuel Fernández-Real, Joan Vendrell, Inmaculada Simón, Cristina Gutierrez and Cristóbal Richart

Endocrinology and Diabetes Unit (A.M., L.G., J.V., I.S., C.G., C.R.), Research Department, University Hospital of Tarragona "Joan XXIII," School of Medicine, Rovira I Virgili University, Tarragona 43007, Spain; and Endocrinology and Diabetes Unit (J.-M.F.-R.), Department of Internal Medicine, University Hospital of Girona "Dr. Josep Trueta," Girona 17007, Spain

Address all correspondence and requests for reprints to: Anna Megia Colet, Secció d’endocrinología, Hospital Universitari "Joan XXIII" de Tarragona, c/Mallafré Guasch, 4.43007 Tarragona, Spain. E-mail: jvo{at}comt.es.

Insulin resistance is a feature of gestational diabetes mellitus (GDM). Inverse correlations between indexes of insulin sensitivity and serum markers of inflammation have been observed and, particularly, TNF-{alpha} has been shown to be associated with the appearance of insulin resistance in pregnancy. Mannose-binding lectin (MBL) is a protein member of the collectin family. Its deficiency is genetically determined and predisposes to recurrent infections and chronic inflammatory diseases. To test the hypothesis that a genetic predisposition to a proinflammatory state could favor the appearance of GDM during pregnancy, we studied R52C and G54D polymorphisms of MBL2 gene and plasma MBL levels from 105 consecutive GDM women and 173 healthy pregnant women. An association was found between G54D and GDM [odds ratio, 2.03 (1.18–3.49); P < 0.01], and this association remained significant when the presence of both mutated alleles was considered [odds ratio, 1.76 (1.04–2.96); P < 0.05] but not for the R52C. GDM patients who carried the G54D mutation required insulin therapy more frequently (56.4 vs. 30.4%, {chi}2 =5.83; P = 0.027) and had heavier infants (3326.4 ± 546.9 vs. 3087.5 ± 395.5 g; P < 0.05) than GDM women homozygous for the wild-type allele. An inverse correlation in GDM patients between neonatal weight and plasma MBL levels (r = –0.320; P = 0.002) was found, remaining significant after adjustment for confounding variables. In conclusion, pregnant women bearing the G54D MBL allele have a greater risk for developing GDM and having heavier infants.




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