Effect of Vaspin on insulin resistance in gestational diabetes and the involvement of the ROS/eNOS/NO pathway.

The global prevalence of gestational diabetes mellitus (GDM) is increasing, posing significant health risks to both mothers and infants. Visceral adipose tissue-derived serine protease inhibitor (Vaspin) has been identified as a potential insulin sensitizer that may mitigate insulin resistance (IR). However, the related mechanism by which Vaspin improves IR in patients with GDM remains unclear. This study aims to investigate whether Vaspin ameliorates IR in GDM via modulation of the ROS/eNOS/NO signaling pathway. Clinical samples from 58 pregnant women were collected and categorized into GDM and control (G) groups. Binary logistic regression analysis revealed significant associations between Vaspin, IR, and GDM. A GDM rat model was established using 50 female Sprague-Dawley (SD) rats, divided into GDM and G groups. Fasting blood glucose (FBG), fasting insulin (FINS), and Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) levels were measured using ELISA and steady-state model evaluation. Vaspin intervention significantly reduced FBG, FINS, and HOMA-IR levels in the GDM group, while L-NAME, an endothelial nitric oxide synthase (eNOS) inhibitor, blocked these effects. INS-1 cells were used to establish a high-glucose model, and laser confocal microscopy, ELISA, and Griess reagent were employed to detect reactive oxygen species (ROS), eNOS, and nitric oxide (NO) levels. Exogenous Vaspin administration improved ROS, eNOS, and NO levels, but these effects were inhibited by L-NAME. Collectively, these results propose a model in which the protective effect of Vaspin against insulin resistance in GDM may be mediated, at least in part, through the ROS/eNOS/NO pathway.