Association of dietary glycemic index and glycemic load with the risk of gestational diabetes mellitus: a systematic review and dose-response meta-analysis.

OBJECTIVE: To comprehensively assess the dose-response association between dietary glycemic index (GI) and glycemic load (GL) and gestational diabetes mellitus (GDM) risk. METHODS: PubMed, Embase, Cochrane Library, Web of Science, CNKI, WanFang, and VIP databases were searched up to May 29, 2024. Studies with at least three exposure categories were included. Dose-response analysis was also performed when covariates were adjusted in the included studies. RESULTS: Thirteen studies involving 39,720 pregnant women were included. A linear relationship was found between GI and the risk of GDM (χ2 = 4.77, Pnon-linearity = .0923). However, association was not significant (χ2 = 0.06, p = .8000). For every unit increase in GI (range 0-30), GDM risk increased by 0.29%. After adjusting for covariates, the linear relationship persisted (χ2 = 4.95, Pnon-linearity = .084) with no significant association (χ2 = 0.08, p = .7775). For GL, a linear relationship was also found (χ2 = 4.17, Pnon-linearity =.1245), but GL was not significantly associated with GDM risk (χ2 = 2.63, p = .1049). The risk of GDM increased by 0.63% per unit increase in GL. After covariate adjustment, a significant association was observed (χ2 = 6.28, p = .0122). CONCLUSION: No significant association between GI and GDM risk was found. After adjusting for covariates, GL shows a significant association with GDM risk. Our findings emphasize the importance of considering dietary GL in managing the risk of GDM. Future research should continue to explore these relationships with standardized diagnostic criteria and robust adjustment for potential confounders.

Effect of miR-301a/PTEN pathway on the proliferation and apoptosis of cervical cancer.

The aim of this study was to evaluate the effect of the miR-301a/PTEN pathway in cervical cancer. miR-301a and PTEN expression were measured by quantitative real-time PCR (qRT-PCR) in tissues samples and HeLa cells. PTEN protein level was determined by Western blotting. Dual reporter luciferase assay was performed to validate PTEN as a direct target of miR-301a. The gain- and loss-of function assay was performed by miR-301a overexpression and silencing. Cell proliferation was monitored by cell counting Kit-8 (CCK-8). Cell apoptosis was quantitated by flow cytometry. SPSS was used to analyze the significant difference in the treatments. miR-301a demonstrated a significantly higher expression in cervical carcinoma tissues compared with the paired non-carcinoma tissues ( n = 12), while PTEN expression was found to be significantly lower in cervical carcinoma tissues than their paired non-carcinoma tissues ( n = 12). In addition, PTEN was identified as the direct target of miR-301a. Moreover, overexpression of miR-301a significantly promoted HeLa cells proliferation and anti-apoptosis which had a reverse pattern after PTEN overexpression. Our results confirm PTEN as a direct target of miR-301a in HeLa cells and suggest that miR-301a/PTEN pathway contributes to the development and progression of cervical cancer.