AUTHOR=Gao Ming , Li Jing , Zhang Rui , Li Ninghua , Li Weiqin , Zhang Shuang , Wang Peng , Wang Hui , Fang Zhongze , Yu Zhijie , Hu Gang , Leng Junhong , Yang Xilin 

TITLE=Serum mannan-binding lectin-associated serine proteases in early pregnancy for gestational diabetes in Chinese pregnant women

JOURNAL=Frontiers in Endocrinology

VOLUME=Volume 14 - 2023

YEAR=2023

URL=https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2023.1230244

DOI=10.3389/fendo.2023.1230244

ISSN=1664-2392

ABSTRACT=Aims: This study aimed to explore associations of mannan-binding lectin serine proteases (MASPs) levels in early pregnancy with gestational diabetes mellitus (GDM).We also examined interactions of MASPs and deoxycholic acid (DCA)/glycoursodeoxycholic acid (GUDCA) for GDM risk and whether the interactive effects if any on GDM risk were mediated via lysophosphatidylcholines (LPC) 18:0.A 1:1 case-control study (n=414) nested in a prospective cohort of pregnant women was conducted in Tianjin, China. Binary conditional logistic regressions were performed to examine associations of MASPs with GDM risk.Additive interaction measures were used to examine interactions between MASPs and DCA/GUDCA for GDM risk. Mediation analyses and Sobel tests were used to examine mediation effects of LPC18:0 between copresence of MASPs and DCA/GUDCA on GDM risk.Results: High MASP-2 was independently associated with GDM (OR: 2.62, 95%CI:1.44-4.77), while the effect of high MASP-1 on GDM was attributable to high MASP-2 (P for Sobel test: 0.003). Low DCA markedly increased the OR of high MASP-2 alone from 2.53 (1.10-5.85) up to 10.6 (4.22-26.4), with a significant additive interaction. In addition, high LPC18:0 played a significant mediating role in the links from low DCA to GDM and from copresence of high MASP-2 and low DCA to GDM (P for Sobel test <0.001), but not in the link from high MASP-2 to GDM.High MASP-1 & 2 in early pregnancy were associated with GDM in Chinese pregnant women. MASP-2 amplifies the risk of low DCA for GDM, which is mediated via LPC18:0.