Comparison of umbilical cord ghrelin concentrations in full-term pregnant women with or without gestational diabetes.

PURPOSE: Ghrelin is a potent orexigenic peptide hormone secreted from the gastrointestinal tract that plays a crucial role in the regulation of lipids and glucose metabolism. Ghrelin also has links with fetal development and growth. Gestational diabetes mellitus (GDM) causes fetal macrosomia, but there is no available evidence of a relationship between ghrelin levels and birth weight in women with GDM. The purpose of this study is to investigate whether umbilical cord ghrelin concentrations are altered in full-term pregnant women with GDM compared to women without GDM and whether birth weight is correlated with ghrelin levels. MATERIALS AND METHODS: Sixty pregnant women with GDM and 64 healthy pregnant women without GDM were included in this cross-sectional study. Blood samples were drawn from the umbilical vein following birth. Ghrelin concentrations were measured using enzyme-linked immunosorbent assay (ELISA). RESULTS: Umbilical vein ghrelin levels were decreased in women with GDM (879.6 ± 256.1 vs. 972.2 ± 233.6 pg/ml in women without GDM, p=0.033), whereas birth weights were higher for babies in the GDM than in the non-GDM group (3448 ± 410 vs. 3308 ± 365 gr, respectively, p=0.046). Umbilical ghrelin levels were inversely correlated with birth weight (r=-0.765, p<0.001). Multiple regression analysis revealed that birth weight was independently and negatively associated with umbilical ghrelin levels (ß= -2.077, 95% CI=-2.652 to -1.492, p=0.002). CONCLUSIONS: Umbilical ghrelin levels were lower in GDM women. Birth weight was inversely associated with umbilical ghrelin levels. This association may be explained by a negative feedback mechanism between ghrelin and birth weight.

Increased circulating urocortin-3 levels is associated with polycystic ovary syndrome.

This study was aimed to compare serum urocortin-3 (UCN3) levels in women with polycystic ovary syndrome (PCOS) and healthy women, and establish what role UCN3 levels play in PCOS. Fifty-two patients with PCOS and 55 healthy women were included in the study, matched for age and body mass index. Fasting blood glucose (FBG), insulin, hs-CRP, UCN3 and free-testosterone levels of the all participants were measured. HOMA-IR was used to calculate the insulin resistance. Circulating UCN3 levels were significantly increased in women with PCOS than in control subjects (54.49 ± 5.77 versus 51.28 ± 5.86 pmol/l, p = 0.005). Serum insulin, hs-CRP and HOMA-IR levels were higher in women with PCOS than in control group. UCN3 levels positively correlated with hs-CRP in PCOS group (r = 0.391, p = 0.004). Receiver operating characteristic (ROC) curve analysis showed that the area under the ROC curves were 0.732 (95% CI 0.634-0.830, p < 0.001) for UCN3 levels. The optimal cut-off value of UCN3 for detecting PCOS was ≥51.46 pmol/l, at which the sensitivity was 75% and specificity was 68%. Our results suggest that there is a potential link between PCOS and UCN3 levels. The results of this study support the presence of increased UCN3 levels for the association of inflammation with PCOS.

The relationship between lipocalin-2 and free testosterone levels in polycystic ovary syndrome.

INTRODUCTION: Lipocalin-2 is an adipokine that is mainly produced from adipocytes and macrophages. Data related to PCOS and other obesity-associated disorders have shown divergent results. Here, we studied lipocalin-2 concentrations in women with PCOS and in healthy women, and investigated the potential contributors underlying lipocalin association with PCOS. MATERIAL AND METHODS: Forty-four women with PCOS and 47 age- and BMI-matched healthy women were enrolled. Fasting serum glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), high-sensitivity C-reactive protein (hs-CRP), and free testosterone levels were measured. The body fat percentage was measured by bioelectrical impedance. RESULTS: Lipocalin-2 concentrations were significantly higher in the PCOS group than in the control group (55.74 ± 17.54 ng/mL vs. 36.46 ± 19.62 ng/mL, p = 0.011). There was a correlation between lipocalin-2 levels and free testosterone. In a multiple regression model, the body fat percentage, HOMA-IR, and hs-CRP were not associated with lipocalin-2. However, only free testosterone was associated with lipocalin-2. A "lipocalin-2 = 11.214 + (1.943 × free-testosterone)" equation was obtained. CONCLUSIONS: Serum lipocalin-2 levels were higher in women with PCOS, and only free testosterone was associated with lipocalin-2. Lipocalin-2 levels and their influencing factors have discrepant results in both PCOS and other obesity- or insulin resistance-related metabolic disorders. Thus, the potential role of lipocalin-2 in PCOS should be clarified. (Endokrynol Pol 2017; 68 (1): 7-12).