Related Experiment Video
Updated: Jan 15, 2026

A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
Published on: June 24, 2020
Maresin-1 and S-Equol as Emerging Metabolic Biomarkers in Gestational Diabetes-Associated Inflammation
Seyda Yavuzkir1, Derya Kardas Cinar2, Ahmet Cinar2
1Department of Obstetrics and Gynecology, Medical School, Firat University, Elazig 23119, Turkey.
Background/Objectives: The most prevalent metabolic condition during pregnancy is gestational diabetes mellitus (GDM), typically diagnosed in the second or third trimester and absent prior to gestation, with a reported prevalence ranging between 1% and 14%. Although the pathogenesis of GDM is thought to involve increased insulin resistance, impaired beta-cell function and mass, and a heightened inflammatory state, the underlying pathophysiological mechanisms remain incompletely understood. Thus, the purpose of this study was to look into any possible relationships between GDM and particular inflammatory biomarkers (Maresin-1 [MaR-1], high-sensitivity-C-reactive protein [Hs-CRP]) as well as microbiota-derived metabolites (Trimethylamine-N-oxide [TMAO], S-Equol, and Indoxyl Sulfate [IS]). Methods: A total of 44 pregnant women were enrolled in this study, comprising 22 women with GDM and 22 healthy pregnant controls. Venous blood samples were collected, and serum levels of TMAO, IS, Hs-CRP, MaR-1, and S-Equol were quantified using enzyme-linked immunosorbent assay (ELISA). Results: Serum levels of MaR-1 and S-Equol were significantly reduced in the GDM group compared to healthy controls (p < 0.05). In contrast, no statistically significant differences were observed in the levels of TMAO, IS, or Hs-CRP between the GDM and control groups (p > 0.05). Conclusions: The observed reductions in MaR-1 and S-Equol levels among GDM patients suggest a potential role for these anti-inflammatory mediators in the inflammatory processes associated with GDM. That is, these findings imply that the advantages of using these MaR-1 and S-Equol could be predictive for GDM.
Background/Objectives: The most prevalent metabolic condition during pregnancy is gestational diabetes mellitus (GDM), typically diagnosed in the second or third trimester and absent prior to gestation, with a reported prevalence ranging between 1% and 14%. Although the pathogenesis of GDM is thought to involve increased insulin resistance, impaired beta-cell function and mass, and a heightened inflammatory state, the underlying pathophysiological mechanisms remain incompletely understood. Thus, the purpose of this study was to look into any possible relationships between GDM and particular inflammatory biomarkers (Maresin-1 [MaR-1], high-sensitivity-C-reactive protein [Hs-CRP]) as well as microbiota-derived metabolites (Trimethylamine-N-oxide [TMAO], S-Equol, and Indoxyl Sulfate [IS]). Methods: A total of 44 pregnant women were enrolled in this study, comprising 22 women with GDM and 22 healthy pregnant controls. Venous blood samples were collected, and serum levels of TMAO, IS, Hs-CRP, MaR-1, and S-Equol were quantified using enzyme-linked immunosorbent assay (ELISA). Results: Serum levels of MaR-1 and S-Equol were significantly reduced in the GDM group compared to healthy controls (p < 0.05). In contrast, no statistically significant differences were observed in the levels of TMAO, IS, or Hs-CRP between the GDM and control groups (p > 0.05). Conclusions: The observed reductions in MaR-1 and S-Equol levels among GDM patients suggest a potential role for these anti-inflammatory mediators in the inflammatory processes associated with GDM. That is, these findings imply that the advantages of using these MaR-1 and S-Equol could be predictive for GDM.
Related Concept Videos
Diabetes Mellitus: Type 2 and Gestational
Pathophysiology of Diabetes
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility,...

