Ebert Thomas, Kralisch Susan, Wurst Ulrike, Lössner Ulrike, Kratzsch Jürgen, Blüher Matthias, Stumvoll Michael, Tönjes Anke, Fasshauer Mathias
Department of Endocrinology and NephrologyUniversity of Leipzig, Liebigstraße 20, 04103 Leipzig, GermanyLeipzig University Medical CenterIFB AdiposityDiseases, Liebigstraße 20, 04103 Leipzig, GermanyInstitute of Laboratory MedicineUniversity of Leipzig, Leipzig, Germany Department of Endocrinology and NephrologyUniversity of Leipzig, Liebigstraße 20, 04103 Leipzig, GermanyLeipzig University Medical CenterIFB AdiposityDiseases, Liebigstraße 20, 04103 Leipzig, GermanyInstitute of Laboratory MedicineUniversity of Leipzig, Leipzig, Germany
Department of Endocrinology and NephrologyUniversity of Leipzig, Liebigstraße 20, 04103 Leipzig, GermanyLeipzig University Medical CenterIFB AdiposityDiseases, Liebigstraße 20, 04103 Leipzig, GermanyInstitute of Laboratory MedicineUniversity of Leipzig, Leipzig, Germany Department of Endocrinology and NephrologyUniversity of Leipzig, Liebigstraße 20, 04103 Leipzig, GermanyLeipzig University Medical CenterIFB AdiposityDiseases, Liebigstraße 20, 04103 Leipzig, GermanyInstitute of Laboratory MedicineUniversity of Leipzig, Leipzig, Germany.
Eur J Endocrinol. 2015 Jul;173(1):1-7. doi: 10.1530/EJE-14-0815. Epub 2015 Apr 7.
Betatrophin has recently been introduced as a novel adipokine/hepatokine, which promotes pancreatic β cell proliferation and improves glucose tolerance in several mouse models of insulin resistance. However, regulation of betatrophin in gestational diabetes mellitus (GDM), as well as its association with markers of obesity, such as glucose and lipid metabolism, inflammation, and renal function, have not been elucidated.
Circulating betatrophin was quantified in 74 women with GDM and 74 healthy and gestational age-matched controls by ELISA. In a subset of the study population comprising of 85 patients (41 previous controls, 44 previous women with GDM), postpartum betatrophin levels were measured in a follow-up study.
Median (interquartile range) serum betatrophin levels were higher in women with GDM (1.79 (0.53) μg/l) as compared to non-diabetic pregnant controls (1.58 (0.44) μg/l) (P=0.002). In multivariate analysis, GDM status was an independent and positive predictor of circulating betatrophin (P=0.001). Furthermore, betatrophin levels were significantly higher during gestation (1.70 (0.53) μg/l) as compared to postpartum levels (1.55 (0.66) μg/l) (P=0.028). Moreover, postpartum irisin remained a positive and independent predictor of postpartum betatrophin concentrations.
Women with GDM have significantly higher betatrophin levels as compared to healthy pregnant controls and GDM status positively predicts circulating betatrophin. Furthermore, postpartum levels are significantly lower as compared to betatrophin concentrations during pregnancy. Moreover, irisin is a significant predictor of postpartum betatrophin levels.
β-促细胞生成素最近被作为一种新型脂肪因子/肝脏因子引入，它能促进胰腺β细胞增殖，并在多种胰岛素抵抗小鼠模型中改善葡萄糖耐量。然而，妊娠期糖尿病（GDM）中β-促细胞生成素的调节及其与肥胖标志物（如糖脂代谢、炎症和肾功能）的关联尚未阐明。
采用酶联免疫吸附测定法（ELISA）对74例GDM女性患者和74例健康且孕周匹配的对照者的循环β-促细胞生成素进行定量分析。在包括85名患者（41名先前的对照者，44名先前的GDM女性患者）的研究人群亚组中，进行了一项随访研究以测量产后β-促细胞生成素水平。
与非糖尿病孕妇对照组（1.58（0.44）μg/l）相比，GDM女性患者的血清β-促细胞生成素水平中位数（四分位间距）更高（1.79（0.53）μg/l）（P = 0.002）。多因素分析显示，GDM状态是循环β-促细胞生成素的独立且正向预测因子（P = 0.001）。此外，与产后水平（1.55（0.66）μg/l）相比，孕期β-促细胞生成素水平显著更高（1.70（0.53）μg/l）（P = 0.028）。此外，产后鸢尾素仍是产后β-促细胞生成素浓度的正向且独立预测因子。
与健康孕妇对照组相比，GDM女性患者的β-促细胞生成素水平显著更高，且GDM状态正向预测循环β-促细胞生成素。此外，产后水平与孕期β-促细胞生成素浓度相比显著更低。此外，鸢尾素是产后β-促细胞生成素水平的重要预测因子。
