Maternal serum adipokines and inflammatory markers at late gestation and newborn weight in mothers with and without gestational diabetes mellitus

Abstract

Objectives: Maternal obesity increases the risk of gestational diabetes mellitus (GDM) and is positively correlated with neonatal obesity increasing the risk of adiposity in both young and adult offspring. Maternal secreted factors from adipose tissue such as adipokines and inflammatory cytokines may regulate fetal growth. This study investigated associations between maternal adipokines and inflammatory markers at late gestation, and neonatal anthropometric characteristics in mothers with and without GDM. Material and methods:The study included 65 women with GDM and 65 pregnant women with normal glucose tolerance evaluated at the time of term elective Caesarean section.Adiponectin, leptin, resistin, adipsin, neutrophil gelatinase-associated lipocalin (NGAL), nerve growth factor (NGF), monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha) concentrations were measured in maternal serum by the multiplex immunoassay using Magpix technology. C-reactive protein (CRP) was measured with a particle-enhanced turbidimetric immunoassay and neonatal anthropometric variables were assessed. The association of birthweight with individual biomarkers was analyzed using multivariate logistic regression adjusted for maternal factors.Results: Adiponectin, leptin, resistin, adipsin, NGAL and NGF were not significantly associated with higher birthweight. The maternal factors in association with higher birthweight observed in GDM were CRP, MCP-1 and TNF-alpha levels. Regression analysis showed that TNF-alpha was an independent risk factor for higher birthweight (p = 0.046).Conclusions: These results suggest an involvement of maternal inflammatory markers at late gestation and fetal growth in mothers with GDM, and that TNF-alpha could play a major role.

Association Of Blood Lipocalin-2 Levels with Gestational Diabetes Mellitus: A Systematic Review and Meta-Analysis

“…Overall, 15 studies with 1882 individuals were included. The studies were performed in Denmark 16 , Italy 15 , Mexico 17 , Poland 24 , and China 4 12 23 25 26 27 28 29 30 . All included studies were case-control studies and five were nested case-control studies.…”

“…The unknown sources and structural diversity of the variants of LCN2 lead to significant variabilities for clinical assessment [48]. LCN2 levels in most studies included were tested by ELISA, the difference between subjects with GDM and subjects in the control group were significant, whereas two studies [16,17] using other methods did not show the same trend. According to recent reviews, there is currently no "gold standard" method for detecting and measuring LCN2.…”

“…Recent evidence points to the role of LCN2 in the pathophysiology of GDM. Although a previous study proposed that blood LCN2 were higher in patients with GDM compared with parturients with normal glucose tolerance (NGT) [15], subsequent studies showed inconsistent results [16,17]. Since the existing results from accessible studies are conflicting, evidence-based quantitative analyses evaluating the correlation between circulating LCN2 levels and GDM are indispensable.…”

Features of Adiponectin at the Mother–placenta–fetus System

“…Данные многих исследователей показали, что ГСД связан с ростом гипертрофических адипоцитов, которые за счет синтеза провоспалительных и ангиогенных факторов подавляют транскрипцию гена адипонектина и ведут к значительному снижению его концентрации в плазме крови, что приводит к инсулинорезистентности и, как следствие, к повышению уровня глюкозы в крови [17,19,20,54]. При ожирении адипоциты также синтезируют большое количество провоспалительных цитокинов [51,55].…”

A positive association of serum CCN5/WISP2 levels with the risk of developing gestational diabetes mellitus: a case–control study

“…Offspring born to mothers diagnosed with GDM are susceptible to developing jaundice, polycythemia, hypocalcemia, respiratory distress syndrome, and hypoglycemia are more likely to suffer from diabetes and obesity in their adult years [4][5][6]. Notably, changes in the levels of steroid hormones (e.g., cortisol, progesterone, estrogen) and placental hormones (e.g., placental lactogen hormone) can exacerbate insulin resistance [3,7].…”