Getting too sweet: galectin-1 dysregulation in gestational diabetes mellitus

Author(s):Show less -

Blois, Sandra M. ^[1] ; Gueuvoghlanian-Silva, Barbara Y. ^{[2, 3]} ; Tirado-Gonzalez, Irene ^[1] ; Torloni, Maria R. ^[2] ; Freitag, Nancy ^[1] ; Mattar, Rosiane ^[2] ; Conrad, Melanie L. ^[1] ; Unverdorben, Laura ^[4] ; Barrientos, Gabriela ^[1] ; Knabl, Julia ^[4] ; Toldi, Gergely ^[5] ; Molvarec, Attila ^[6] ; Rose, Matthias ^[1] ; Markert, Udo R. ^[3] ; Jeschke, Udo ^[4] ; Daher, Silvia ^[2]

Affiliation

^[1] Med Univ Berlin, Reprod Med Res Grp, Charite Ctr Internal Med & Dermatol 12, Berlin - Germany

^[2] Univ Fed Sao Paulo, Dept Obstet, Sao Paulo - Brazil

^[3] Univ Hosp Jena, Dept Obstet, Placenta Lab, Jena - Germany

^[4] Univ Munich, Dept Obstet & Gynecol, Munich - Germany

^[5] Semmelweis Univ, Dept Pediat 1, H-1085 Budapest - Hungary

^[6] Semmelweis Univ, Dept Obstet & Gynecol 1, H-1085 Budapest - Hungary

• Document type: Review article
• Source: MOLECULAR HUMAN REPRODUCTION; v. 20, n. 7, p. 644-649, JUL 2014.
• Web of Science Citations: 8

Abstract

Galectin-1 (gal-1) 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-1 protein production or gene regulation can be caused by single-nucleotide polymorphisms in the LGALS1 gene. Gestational diabetes mellitus (GDM) is also an adverse pregnancy outcome and the most common metabolic disorder during gestation. However, gal-1 expression patterns during GDM remain largely unknown. Our aims were to define local and peripheral gal-1 expression patterns during pregnancy, and to investigate LGALS1 gene polymorphisms in GDM patients. Circulating gal-1 levels were determined by ELISA in GDM patients and normal pregnant controls, and LGALS1 gene polymorphisms were assessed for association with GDM. Placental tissues were collected from control and GDM term pregnancies to evaluate local gal-1 expression by immunofluorescence. Our results show that GDM is associated with a failure to increase circulating gal-1 levels during the second and third trimester, as well as overexpression of gal-1 in placental tissue. Additionally, the LGALS1 polymorphism rs4820294 was associated with the development of GDM. In pregnancies complicated by GDM, we observed gal-1 dysregulation both locally in the placenta and peripherally in the circulation. Furthermore, the association between the LGALS1 polymorphism and GDM may indicate a genetic contribution to this adverse pregnancy outcome. (AU)

• FAPESP's process: 11/14554-2 - Evaluation of the role of galectin-1 in gestational Diabetes mellitus
• Grantee: Silvia Daher
• Support Opportunities: Regular Research Grants