Bozkurt Latife, Göbl Christian S, Baumgartner-Parzer Sabina, Luger Anton, Pacini Giovanni, Kautzky-Willer Alexandra
Department of Internal Medicine III, Division of Endocrinology and Metabolism, Unit of Gender Medicine, Medical University of Vienna, Vienna, Austria.
Department of Obstetrics and Gynecology, Division of Feto-Maternal Medicine, Medical University of Vienna, Vienna, Austria.
Int J Endocrinol. 2018 Jul 15;2018:5463762. doi: 10.1155/2018/5463762. eCollection 2018.
There is scarce information on associations of adipokines, and concurrent glucose disposal during early pregnancy as performance of oral glucose tolerance is uncommon before 24th gestational week. We sought to examine associations of leptin and adiponectin to insulin sensitivity already at early pregnancy before recommended screening for GDM and to describe trajectories of adiponectin in relation to GDM status.
216 pregnant women were prospectively included at 16th (IQR: 14-18) gestational week (GW) for fasting adiponectin and leptin with subsequent OGTT testing for evaluation of insulin sensitivity and -cell function. Follow-ups of adiponectin were performed at further four visits until 8-12 weeks after delivery.
In early pregnancy, differences in adiponectin and leptin were significant between GDM women ( = 82) and controls ( = 134), whereby those with early GDM (<21st week, = 49) showed more distinguishing levels (adiponectin: 8.5 ± 3.8 versus 10.4 ± 4.4 g/ml, = 0.004; leptin 93.4 ± 38.5 versus 78.0 ± 39.2 g/ml, = 0.005). Both adipokines were significantly associated with insulin sensitivity and -cell function. Their attribution for GDM prediction was moderate to fair and more enhanced in early GDM. Trajectories of adiponectin remained constantly lower in GDM women, whereas dynamics in controls showed initially increased concentrations with decreasing tendency until 3rd trimester. After delivery, low adiponectin was associated with glucose dysregulation.
Associations of adiponectin and leptin with features of deteriorated glucose metabolism at early gestation may be indicative for the endocrine involvement of adipose tissue in the manifestation of GDM and thus predictive for later impairments in metabolic flexibility in women at risk.
关于脂肪因子的关联以及妊娠早期同时进行葡萄糖处理的信息稀缺，因为在妊娠第24周之前进行口服葡萄糖耐量试验的情况并不常见。我们试图在推荐进行妊娠期糖尿病（GDM）筛查之前的妊娠早期，研究瘦素和脂联素与胰岛素敏感性的关联，并描述脂联素与GDM状态相关的变化轨迹。
前瞻性纳入216名孕妇，在妊娠第16周（四分位间距：14 - 18周）测定空腹脂联素和瘦素，随后进行口服葡萄糖耐量试验以评估胰岛素敏感性和β细胞功能。在产后8 - 12周内的另外四次随访中对脂联素进行跟踪。
在妊娠早期，GDM女性（n = 82）和对照组（n = 134）之间脂联素和瘦素存在显著差异，其中早期GDM（<21周，n = 49）患者表现出更明显的水平差异（脂联素：8.5±3.8 vs 10.4±4.4μg/ml，P = 0.004；瘦素93.4±38.5 vs 78.0±39.2μg/ml，P = 0.005）。两种脂肪因子均与胰岛素敏感性和β细胞功能显著相关。它们对GDM预测的归因中等至良好，且在早期GDM中更强。GDM女性的脂联素变化轨迹持续较低，而对照组的动态变化显示最初浓度升高，直至孕晚期呈下降趋势。产后，低脂联素与葡萄糖代谢失调有关。
脂联素和瘦素与妊娠早期葡萄糖代谢恶化特征的关联可能表明脂肪组织的内分泌参与了GDM的发生，从而对有风险女性后期代谢灵活性的损害具有预测作用。
