Low placental visfatin expression is related to impaired glycaemic control and fetal macrosmia in pregnancies complicated by type 1 diabetes.

Type 1 diabetes mellitus (T1DM) is still related to altered fetal growth and severe maternal complications. We studied the possible role of placental visfatin/nicotinamide phosphoribosyltransferase (NAMPT) in fetal development in T1DM pregnancies, the possible role of placental visfatin in fetal macrosomia. Sixty five pregnant women with T1DM and singleton pregnancy were qualified into the study. Placental visfatin expression was by analysed by RT-PCR. We demonstrated the lowest expression of placental visfatin in women who delivered neonates with birth weight NBW > 4000 g (0.76 ± 0.05, P < 0.055). The highest placental visfatin/nicotinamide phosphoribosyltransferase (NAMPT) expression was found in the women who delivered small for gestational age (SGA) and large for gestational age (LGA) newborns (1.09 ± 0.95 vs. 0.87 ± 0.67, P < 0.05, respectively). There was also significant negative correlation between placental visfatin (NAMPT) expression and metabolic status in the 3rd trimester of pregnancy in T1DM LGA group, defined as long-term glycaemic control (3rd trimester HbA1C) - Pearson rank R - 08667654, P < 0.034. We conclude that the low placental visfatin (NAMPT) expression and poor metabolic control in the 3rd trimester of pregnancy may have a role in stimulating fetal overgrowth in T1DM pregnancy.