Getting too sweet: Galectin-I dysregulation in gestational diabetes mellitus

Abstract

Galectin-I (gal-I) is a prototype carbohydrate-binding protein, whose dysregulation is associated with adverse pregnancy outcomes such as spontaneous abortion and pre-eclampsia. Furthermore, it is known that faulty gal-I protein production or gene regulation can be caused by single-nucleotide polymorphisms in the LGALSI gene. Gestational diabetes mellitus (GDM) is also an adverse pregnancy outcome and the mostcommonmetabolic disorder during gestation.However, gal-I expression patterns duringGDMremain largely unknown. Ouraimswere to define local and peripheral gal-I expression patterns during pregnancy, and to investigate LGALSI gene polymorphisms in GDM patients. Circulating gal-I levels were determined by ELISA in GDM patients and normal pregnant controls, and LGALSI gene polymorphisms were assessed for association with GDM. Placental tissues were collected from control and GDM term pregnancies to evaluate local gal-I expression by immunofluorescence. OurresultsshowthatGDMis associated with a failure to increase circulating gal-I levels during the second and third trimester, as well as overexpression of gal-I in placental tissue. Additionally, the LGALSI polymorphism rs4820294 was associated with the development of GDM. In pregnancies complicated by GDM, we observed gal-I dysregulation both locally in the placenta and peripherally in the circulation. Furthermore, the association between the LGALSI polymorphism andGDMmay indicate a genetic contribution to this adverse pregnancy outcome. © The Author 2014. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved.