Interaction between smoking during pregnancy and gestational diabetes mellitus and the risk of cesarean delivery: evidence from the National Vital Statistics System 2019.

OBJECTIVE: To explore the interaction between smoking during pregnancy (SDP) and gestational diabetes mellitus (GDM) on the risk of cesarean delivery. METHODS: This retrospective cohort study utilized data from the National Vital Statistics System (NVSS) 2019. The NVSS database provides data on births and deaths as well as maternal characteristics in the United States. The duration of follow-up was 38.74 ± 2.12 weeks. The outcome was the method of delivery, including vaginal and cesarean delivery. The multivariate logistic regression model was adopted to assess the associations of SDP and GDM with the method of delivery. The interaction between SDP and GDM was examined via calculating the relative excess risk of interaction (RERI), the attributable proportion of interaction (API) and the synergy index (S). Subgroup analyses were conducted based on age, race, prepregnancy body mass index (BMI), and primiparity. RESULTS: The study included 3352615 puerperae. Compared with women who did not smoke during pregnancy, those who smoked during pregnancy had a significantly higher risk of cesarean delivery [odds ratio (OR)=1.07, 95% confidence intervals (CI): 1.05-1.10, p < 0.001]; women with GDM had a significantly greater risk of cesarean delivery than those without (OR = 1.31, 95%CI: 1.30-1.33, p < 0.001). In contrast to women who did not smoke during pregnancy and did not have GDM, those who smoked during pregnancy and had GDM exhibited an increased risk of a cesarean section (OR = 1.47, 95%CI: 1.40-1.54, p < 0.001). RERI was 0.08 (95%CI: 0.01-0.15), API was 0.06 (95%CI: 0.01-0.10), and S was 1.21 (95%CI: 1.04-1.40) suggested that there was an interaction between SDP and GDM, and it was a synergistic effect. There was a synergism between SDP and GDM in women of non-advanced age (RERI = 0.07, 95%CI: 0.001-0.15; API = 0.05, 95%CI: 0.003-0.10; S = 1.17, 95%CI: 1.001-1.36), in white women (RERI = 0.08, 95%CI: 0.004-0.16; API = 0.05, 95%CI: 0.01-0.10; S = 1.19, 95%CI: 1.02-1.39), in women who were overweight before pregnancy (RERI = 0.13, 95%CI: 0.05-0.21; API = 0.08, 95%CI: 0.04-0.13; S = 1.33, 95%CI: 1.14-1.55), and in primiparae (RERI = 0.20, 95%CI: 0.08-0.31; API = 0.12, 95%CI: 0.06-0.19; S = 1.50, 95%CI: 1.23-1.84). CONCLUSION: SDP and GDM were associated with an increased risk of cesarean delivery, and a synergistic effect existed between SDP and GDM on the risk of cesarean delivery, especially in women of non-advanced age, white women, women who were overweight before pregnancy, and primiparae.

LncRNA ANRIL Silencing Alleviates High Glucose-Induced Inflammation, Oxidative Stress, and Apoptosis via Upregulation of MME in Podocytes.

Diabetic nephropathy (DN), characterized by glomerular injury, is a common complication of both type 1 and type 2 diabetes, accompanied by massive proteinuria. Podocytes are reported to play pivotal roles in maintaining the glomerular filtration barrier. In addition, the expression of long non-coding RNAs (lncRNAs) ANRIL was upregulated in type 2 diabetes patients. Hence, the aim of this study was to investigate the underlying mechanisms implicated the role of LncRNA ANRIL in podocyte injury in DN. The concentration of inflammatory cytokines was quantified by the corresponding enzyme-linked immunosorbent assay (ELISA) kits. The mRNA levels of the target gene were determined by reverse transcription and real-time quantitative PCR (RT-qPCR). The expressions of proteins were evaluated by Western blot. The activities of lactate dehydrogenase (LDH), superoxide dismutase (SOD), and malondialdehyde (MDA) level were measured by corresponding commercial kits. Finally, the apoptosis of podocytes was analyzed by TUNEL assay. In our study, LncRNA ANRIL was highly expressed in high glucose (HG)-induced podocytes. Moreover, LncRNA ANRIL silencing attenuated HG-induced inflammation, oxidative stress, and apoptosis and induced MME overexpression in podocytes. Interestingly, MME knockdown abolished the suppressive effect of LncRNA ANRIL silencing on HG-induced inflammation, oxidative stress, and apoptosis in podocytes. LncRNA ANRIL silencing alleviates HG-induced inflammation, oxidative stress, and apoptosis via upregulation of MME in podocytes. Hence, LncRNA ANRIL may be a novel and effective target to ameliorate podocyte injury in DN.