Serum Human Placental Lactogen and Prolactin May Not Be Associated with Aberrant Glucose Homeostasis in GDM

Abstract

Background: Gestational diabetes mellitus (GDM) shows insufficient β-cell compensation for insulin resistance (IR) during late pregnancy, whereupon derangements of human placental lactogen (hPL) and prolactin (PRL) have a presumed role in its pathogenesis. Aims: To assess the relationship of serum hPL and PRL with IR and β-cell function in GDM and pregnant women with normal glucose tolerance (NGT). Materials and Methods: This cross-sectional study was performed with 40 women with GDM and an equal number of pregnant women with NGT who were diagnosed on the basis of the WHO 2013 criteria during 24–40 weeks of gestation. hPL was measured by an enzyme-linked immunosorbent assay (ELISA); PRL and fasting insulin were measured by a chemiluminescent immunoassay. Equations of homeostatic model assessment (HOMA) were used to calculate the indices of IR (HOMA-IR) and β-cell function (HOMA-B). Results: No statistically significant difference was found between the GDM and NGT groups in circulating concentrations of either hPL (6.01 ± 1.76 vs. 5.92 ± 2.10 mg/L, mean ± SD; P = 0.852) or PR [180.27 (125.95–306.20) vs. 166.87 (134.24–284.70) ng/mL, median (IQR); P = 0.704]. There was no relationship of circulatory levels of hPL and PRL with glucose values at different time points during oral glucose tolerance test as well as with AUCglucose (P = NS for all). On multiple regression analysis, neither hPL nor PRL emerged as a significant predictor for fasting insulin, HOMA-IR, and HOMA-B in GDM (P = NS for all). Conclusions: Circulating concentration of hPL and PRL may not be a potential determinant of IR and β-cell dysfunction in GDM.