ObjectiveTo establish a model of fetal hyperglycemia and explore the effects of hyperglycemia on alveolar cell apoptosis,proliferation and the development of lung structure in neonatal rats. MethodsForty SD pregnant rats were randomly divided into a hyperglycemia group (STZ group) and a normal pregnancy group (N group)(n=20 in each group). The rats in STZ group and N group were intraperitoneally injected streptozotocin(STZ,40 mg/kg) or the same bulk of citrate buffer respectively at the 4.5 days after gestation. Blood glucose concentration of the pregnant rats was measured before injection,at the 6.5,11.5,16.5 and 20.5 days after gestation,respectively. The weight,survival rate,lung weight,septal thickness,radical alveolar count,alveolar cell apoptosis and proliferation of neonatal rats were recorded after birth immediately (D0) and at 7 days (D7). ResultsCompared with N group,the blood glucose level increased after intraperitoneal injection of STZ in STZ group (P<0.05). The Survival rate of STZ group was lower than that of N group at D0 and D7 (P=0.00). The neonatal weight,lung weight,septal thickness of STZ group were lower compared with those of N group at D0(P<0.05). However,there was no significant difference between two groups in radical alveolar count. The alveolar apoptosis index of STZ group was higher than that of N group at D0 [(11.8±1.1)% vs. (3.4±0.7)%,P=0.00]. Alveolar cell proliferation significantly increased in STZ group compared with N group at D0 and D7 (P<0.05). ConclusionsThe fetal hyperglycemia model is successfully established by intraperitoneal injection of STZ 40 mg/kg. Fetal hyperglycemia can increase mortality,alveolar cell proliferation and apoptosis,and affect the development of lung structure of neonatal rats.
ObjectiveTo systematically review the preventive effect of breastfeeding intensity and duration on progression to pre-diabetes mellitus (DM) and DM among females with prior gestational diabetes mellitus (GDM).MethodsPubMed, Web of Science, CNKI, and WanFang Data databases were electronically searched to collect cohort studies on the correlation of GDM and breastfeeding from inception to January 8th, 2021. Two reviewers independently screened literature, extracted data, and assessed the risk of bias of included studies. Meta-analysis was then performed using Stata 16.0 software.ResultsA total of 29 cohort studies were included. The results of the meta-analysis showed that breastfeeding could lower the risk of pre-DM (RR=0.64, 95%CI 0.57 to 0.71, P<0.001) and DM (RR=0.75, 95%CI 0.66 to 0.86, P<0.001) among females with prior GDM. Subgroup analysis showed that breastfeeding exhibited protective effects against pre-DM after 0 to 6 months as well as 6 to 12 months. Both breastfeeding for 0 to 6 months and over 12 months could decrease the risk of DM. These effects became prominent with the extension of the follow-up period. However, no significant association was observed between breastfeeding and recurrence of GDM (RR=0.72, 95%CI 0.47 to 1.09, P=0.14).ConclusionsBreastfeeding may be a major contributor in protecting against pre-DM and DM among females with prior GDM history. Due to limited quality and quantity of the included studies, more high-quality studies are needed to verify the above conclusions.
ObjectiveTo systematically evaluate the changes in placental protein expressions in gestational diabetes mellitus (GDM) and their correlations with maternal insulin resistance (IR). Methods PubMed, Cochrane Library, Scopus, Web of Science, Embase, China National Knowledge Infrastructure, VIP database, Wanfang Database and CBMdisc were searched for case-control studies published from January 2009 to November 2021, which reported the placental protein expressions in GDM and their correlations with IR. Two researchers independently reviewed the literature, extracted data and evaluated the literature quality. RevMan 5.4 software was used for meta-analysis, and descriptive analysis was performed on data that cannot be combined. ResultsA total of 19 studies were included, comprising 2 012 patients. The results of meta-analysis showed that: the expression level of retinol binding protein 4 (RBP4) [standard mean difference=2.11, 95% confidence interval (CI) (1.64, 2.58), P<0.000 01] and the positive rate of protein tyrosine phosphatase-1B (PTP1B) [relative risk (RR)=1.56, 95%CI (1.29, 1.88), P<0.000 01] were up-regulated, and the positive rate of insulin receptor substrate 1 (IRS-1) [RR=0.69, 95%CI (0.60, 0.78), P<0.000 01] was down-regulated. The protein expression levels of RBP4 (P<0.000 01) and PTP1B (P<0.000 01) were positively correlated with homeostasis model assessment of insulin resistance (HOMA-IR), while the protein expression levels of IRS-1 (P<0.000 01) and APN (P=0.002) were negatively correlated with HOMA-IR, and glucose transporter 4 (GLUT 4) was not correlated with HOMA-IR (P=0.79). Descriptive analysis found that the expression levels or positive rates of adipocytokines (leptin, resistin), oxidative stress markers (xanthione oxidase, malondialdehyde, 8-isoprostaglandin),inflammatory factors (tumor necrosis factor α, Toll-like receptor 4, Galectin-3, Galectin-2, migration inhibitory factor),fetuin-A, forkhead box transcription factor 1, forkhead box transcription factor 3a and estrogen receptor α in GDM placenta were up-regulated and all were positively correlated with HOMA-IR. The expression levels or positive rates of insulin signaling pathway proteins [phosphoinositide 3-kinase (PI3K), protein kinases B (AKT), phospho-protein kinases B (p-AKT), GLUT 4] were down-regulated, PI3K and AKT were negatively correlatedwith HOMA-IR, while p-Akt had no correlation with HOMA-IR. ConclusionsThe dysregulation of placental protein expressions may mediate maternal IR exacerbation, thus promote the occurrence and development of GDM and other pregnancy complications. The causal relationship and regulatory mechanism are still unclear, which need to be further studied.
ObjectiveTo systematically review the research status of risk prediction models for gestational diabetes mellitus (GDM). MethodsThe CNKI, WanFang Data, VIP, CBM, PubMed, JBI EBP, Ovid MEDLINE, Embase, Web of Science and Cochrane Library databases were electronically searched to collect relevant literature on risk prediction models for GDM from inception to October 2022. Two researchers independently screened the literature, extracted data, and assessed the risk of bias of the included studies, and then qualitative description was performed. ResultsA total of 19 studies were included, involving 19 risk prediction models. The evaluation results showed that, in terms of the risk of bias, 18 studies were high risk, and 1 study was unclear. In terms of applicability, 14 studies were high risk, 2 studies were low risk, and 3 studies were unclear. The area under the receiver operating characteristic curve of the included models was 0.69 to 0.88. The most common predictors included age, weight, pre-pregnancy BMI, history of diabetes, family history of diabetes, and race. ConclusionThe overall performance of the risk prediction model for gestational diabetes mellitus is good, but the risk of bias of the model is high, and the clinical applicability of the model needs to be further verified.