In China, gestational diabetes mellitus (GDM) is typically diagnosed using the International Association of Diabetes and Pregnancy Study Groups (IADPSG) criteria. This study retrospectively analyzed 19152 pregnant women who underwent an oral glucose tolerance test between 2015 and 2021, comparing the IADPSG and the National Institute for Health and Care Excellence (NICE) criteria. GDM prevalence was 20.39% (IADPSG) and 23.67% (NICE, P < 0.01), with a moderate diagnostic agreement (κ = 0.59; P < 0.01). Compared with women having normal glucose tolerance (NGT group), women diagnosed with GDM by either the IADPSG (GDM-I) or NICE (GDM-N) criteria had significantly higher risks of adverse outcomes (including gestational hypertension, preeclampsia, preterm delivery, macrosomia, low birth weight, and neonatal jaundice). However, those diagnosed by NICE but not by IADPSG (GDM-NI) showed no significant increase in adverse maternal or neonatal outcomes except for neonatal jaundice. Furthermore, the GDM-NI group had significantly lower rates of several adverse outcomes compared with the GDM-I group. These findings suggest that, under current clinical management where women diagnosed by IADPSG received treatment while those diagnosed only by NICE did not, the IADPSG criteria classified fewer women as having GDM but identified a group with a higher observed risk of several adverse pregnancy outcomes than did the NICE criteria.

This study aimed to elucidate the protective effect and underlying mechanism of epigallocatechin gallate (EGCG) against high glucose-induced pancreatic β-cell developmental anomalies in zebrafish. Zebrafish embryos were exposed to 2 % glucose to induce abnormal pancreatic β-cell development and were pretreated with 10 μmol/L or 50 μmol/L EGCG. Mortality and body length were recorded; and the expression of key genes related to pancreatic β-cell development and function of pancreatic β-cells was detected by RT-PCR. The morphology of pancreatic β-cells in Tg(ins:mCherry) zebrafish was examined under a fluorescent microscope; and glucose levels, as well as the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), and the levels of malondialdehyde (MDA) and reactive oxygen species (ROS), were measured using commercial kits. The results showed that high-glucose treatment led to an increased mortality rate and body length in zebrafish larvae, along with sustained downregulation in the expression of transcription factors regulating β-cell development. The expression of the insulin a gene (insa) initially increased and then decreased. High-glucose treatment also induced an increase in pancreatic fragmentation and hollow malformations, enlarged islet area, and elevated glucose levels in the body. Furthermore, it caused abnormal activities of SOD, GPx, and CAT enzymes, along with a significant rise in MDA and ROS content in zebrafish larvae. However, intervention with 50 μmol/L EGCG significantly reversed these abnormalities, restored normal β-cell morphology and function, and notably improved the oxidative stress status. In conclusion, EGCG significantly ameliorates high glucose-induced abnormal development of pancreatic β-cells in zebrafish, and its mechanism may be related to the improvement of oxidative stress and glucose levels in zebrafish.