Plasma YKL-40 during pregnancy and gestational diabetes mellitus

Nielsen, Anders Rinnov; Rathcke, Camilla Noelle; Bonde, Lisbeth; Vilsbøll, Tina; Knop, Filip K.

doi:10.1016/j.jri.2015.06.092

Cited by 6 publications

(3 citation statements)

References 25 publications

(50 reference statements)

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“…Two small retrospective cross‐sectional studies of women in late second/early third trimester and third trimester could not find an association between serum YKL‐40 and GDM . However, Schaller et al found a positive correlation between serum YKL‐40 and BMI , which we also found in early pregnancy.…”

Section: Discussioncontrasting

confidence: 50%

“…However, serum YKL‐40 correlated with BMI and HOMA‐IR and a positive correlation was found between serum YKL‐40 and insulin concentrations after 1 and 2 h during an oral glucose tolerance test . Rinnov et al found no differences in plasma YKL‐40 between GDM and non‐GDM pregnant women in the third trimester, but higher HOMA‐IR in the GDM‐group as Schaller et al . No studies have investigated the relation between serum YKL‐40 and GDM in early pregnancy.…”

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confidence: 97%

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Serum YKL‐40 and gestational diabetes – an observational cohort study

Gybel-Brask

Johansen

Christiansen

et al. 2016

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To examine serum YKL-40 in women developing gestational diabetes mellitus (GDM). In the present large observational cohort study of 1179 pregnant women, we determined serum YKL-40 four times during pregnancy (at gestational age 12, 20, 25, and 32 weeks). Pregnancy outcome was obtained from medical records. Sixty-eight women (5.8%) developed GDM. Serum YKL-40 increased from gestational age (GA) 12 weeks and the following weeks in the women who developed GDM and was independent of BMI, parity, and maternal age (OR = 2.69, 95% CI: 1.45-5.00, p = 0.002). No association was found between serum YKL-40 and the oral glucose tolerance test results. In conclusion, YKL-40 significantly increased in pregnant women with GDM compared with women without GDM, probably reflecting the low-grade inflammation of GDM. However, we did not find an association between serum concentrations of YKL-40 in early pregnancy and the development of GDM and thus we conclude that YKL-40 alone is not usable as a biomarker for early prediction of GDM.

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Section: Discussioncontrasting

confidence: 50%

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confidence: 97%

Serum YKL‐40 and gestational diabetes – an observational cohort study

Gybel-Brask

Johansen

Christiansen

et al. 2016

APMIS

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“…22,23 Regarding pregnancy-related disorders, there are several reports on the changes in the concentration of maternal serum CHI3L1 in preeclampsia and gestational diabetes mellitus, the results of which are still controversial. [24][25][26][27][28][29][30][31][32] The CHI3L1 has barely been studied in other pregnancy disorders or normal parturition in which the inflammatory response is crucial, but a cohort study showed the increase in plasma CHI3L1 at midpregnancy was associated with subsequent spontaneous preterm birth. 33 Therefore, we hypothesized that CHI3L1 and Brp-39, a murine homolog of CHI3L1, may play a role in preterm birth due to inflammation and studied the biological significance of Brp-39 during pregnancy.…”

Section: Introductionmentioning

confidence: 99%

Alteration in Uterine Protease-Activated Receptor 2 Expression in Preterm Birth Induced Experimentally in Brp-39 Null Mutant Mice

et al. 2019

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Breast regression protein 39 (Brp-39) is a mouse homolog of human Chitinase 3-like 1, which belongs to the 18-glycosyl-hydrolase family and plays a role in inflammatory reaction and tissue remodeling. The aim of this study is to investigate the role of Brp-39 in a mouse model of preterm birth. Pregnant wild-type (WT) or Brp-39(-/-) mice were injected intraperitoneally with lipopolysaccharide (LPS) at embryonic day 15. Pregnancy outcomes were evaluated for 24 hours after LPS injection. Quantitative real-time polymerase chain reaction and immunoblotting were performed to analyze messenger RNA (mRNA) and protein expressions of cytokines and contraction-associated proteins in uterine and/or placental tissue after LPS injection. LPS injection led to preterm birth in both WT and Brp-39(-/-) mice, but the proportion of pubs delivered was reduced in Brp-39(-/-) mice, along with a longer interval from the LPS injection to delivery, compared to WT mice. Inflammatory cell infiltration and mRNA expression of cytokines and Ptgs2 in the uteri and the placentas were not significantly different between WT and Brp-39(-/-) mice. Par-2 mRNA expression in the WT uteri was increased before delivery after LPS injection and decreased after delivery, while there was no significant change in Par-2 expression in the Brp-39(-/-) uteri. Protein expressions of Par-2 and Ptgs2 were lower in the Brp-39(-/-) uteri than in the WT uteri before and after delivery. Attenuated preterm birth in Brp-39(-/-) mice indicates the significance of Brp-39 during murine preterm birth. Altered expression of Par-2 in Brp-39(-/-) uteri suggests its potential role in attenuated preterm birth of Brp-39(-/-) mice.

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