Relationship between serum NLRP3 along with its effector molecules and pregnancy outcomes in women with hyperglycemia.

OBJECTIVE: The study aims to investigate the levels of serum NLRP3 along with its effector molecules (Caspase-1, IL-1ß, and IL-18) in the mid-pregnancy in pregnant women with hyperglycemia, and explore the relationship between NLRP3, along with its effector molecules (Caspase-1, IL-1ß, and IL-18) and insulin resistance, as well as pregnancy outcomes. METHODS: The levels of serum NLRP3 along with its effector molecules (Caspase-1, IL-1ß, and IL-18) in three groups of pregnant women with gestational diabetes mellitus (GDM), pregestational diabetes mellitus (PGDM) and normal glucose tolerance (NGT) were measured in mid-pregnancy, and their relationship with insulin resistance and pregnancy outcomes was analyzed. The ROC curve was also used to evaluate the predictive value of serum NLRP3 inflammasome and its effector molecules for pregnancy outcomes. RESULTS: There were no statistical differences in the general clinical data of the three groups, and the concentrations of serum NLRP3 along with its effector molecules were higher in the GDM and PGDM groups than in the NGT group, and NLRP3 along with its effector molecules were positively correlated with fasting blood glucose, fasting insulin, and insulin resistance index in both groups (r > 0, p < .05). The incidence of preterm delivery, hypertensive disorders of pregnancy, premature rupture of membranes, neonatal hypoglycemia and macrosomia was significantly higher in both groups than in the NGT group (p < .05). The value of the combined serum NLRP3 and its effector molecules in mid-pregnancy to predict adverse pregnancy outcomes was highest, and the AUCs for the combined prediction of late hypertensive disorders of pregnancy, premature rupture of membranes, preterm delivery, neonatal hypoglycemia and macrosomia were 0.84 (95% CI 0.79-0.88, p < .001), 0.81 (95% CI 0.75-0.85, p < .001), 0.76 (95% CI 0.70-0.81, p < .001), 0.76 (95% CI 0.70-0.81, p < .001) and 0.72 (95% CI 0.63-0.81, p < .001), respectively. CONCLUSIONS: Increased serum NLRP3 along with its effector molecules in pregnant women with hyperglycemia are associated with the levels of insulin resistance and the subsequent development of adverse pregnancy outcomes.

Expression and correlation analysis of silent information regulator 1 (SIRT1), sterol regulatory element-binding protein-1 (SREBP1), and pyroptosis factor in gestational diabetes mellitus.

BACKGROUND AND AIM: Globally, the prevalence of gestational diabetes mellitus (GDM) is rising each year, yet its pathophysiology is still unclear. To shed new light on the pathogenesis of gestational diabetes mellitus and perhaps uncover new therapeutic targets, this study looked at the expression levels and correlations of SIRT1, SREBP1, and pyroptosis factors like NLRP3, Caspase-1, IL-1, and IL-18 in patients with GDM. METHODS: This study involved a comparative analysis between two groups. The GDM group consisted of 50 GDM patients and the control group included 50 pregnant women with normal pregnancies. Detailed case data were collected for all participants. We utilized real-time quantitative PCR and Western Blot techniques to assess the expression levels of SIRT1 and SREBP1 in placental tissues from both groups. Additionally, we employed an enzyme-linked immunosorbent assay to measure the serum levels of SIRT1, SREBP1, and pyroptosis factors, namely NLRP3, Caspase-1, IL-1ß, and IL-18, in the patients of both groups. Subsequently, we analyzed the correlations between these factors and clinical. RESULTS: The results showed that there were significantly lower expression levels of SIRT1 in both GDM group placental tissue and serum compared to the control group (p < 0.01). In contrast, the expression of SREBP1 was significantly higher in the GDM group than in the control group (p < 0.05). Additionally, the serum levels of NLRP3, Caspase-1, IL-1ß, and IL-18 were significantly elevated in the GDM group compared to the control group (p < 0.01). The expression of SIRT1 exhibited negative correlations with the expression of FPG, OGTT-1h, FINS, HOMA-IR, SREBP1, IL-1ß, and IL-18. However, there was no significant correlation between SIRT1 expression and OGTT-2h, NLRP3, or Caspase-1. On the other hand, the expression of SREBP1 was positively correlated with the expression of IL-1ß, Caspase-1, and IL-18, but has no apparent correlation with NLRP3. CONCLUSIONS: Low SIRT1 levels and high SREBP1 levels in placental tissue and serum, coupled with elevated levels of pyroptosis factors NLRP3, Caspase-1, IL-1ß, and IL-18 in serum, may be linked to the development of gestational diabetes mellitus. Furthermore, these three factors appear to correlate with each other in the pathogenesis of GDM, offering potential directions for future research and therapeutic strategies.