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Abstract

Background

To evaluate the diagnostic value of lncRNA SNHG14 and miR-493-5p in gestational diabetes mellitus (GDM).

Methods

This study consisted of 128 GDM patients and 125 healthy controls. Dual luciferase reporter assay detected binding of lncRNA SNHG14 and miR-493-5p. ROC was applied to evaluate the diagnostic value of lncRNA SNHG14 and miR-493-5p for GDM. Independent factors affecting GDM were evaluated using logistic regression analysis. The role of lncRNA SNHG14, miR-493-5p in pregnancy outcome in GDM patients was assessed by chi-square tests.

Results

LncRNA SNHG14 has a target-binding relationship with miR-493-5p. LncRNA SNHG14 was significantly higher in GDM patients, while miR-493-5p was significantly lower; both were independent risk factors for GDM development. Blood glucose indices (fasting, 1 h and 2 h postprandial) were positively correlated with lncRNA SNHG14 and negatively correlated with miR-493-5p in GDM patients. LncRNA SNHG14 in combination with miR-493-5p increased the diagnostic efficiency for GDM. LncRNA SNHG14 was significantly associated with neonatal weight and neonatal jaundice. MiR-493-5p was significantly associated with neonatal jaundice.

Conclusion

LncRNA SNHG14 in combination with miR-493-5p may be an early diagnostic marker of GDM. LncRNA SNHG14 and miR-493-5p are associated with adverse pregnancy outcomes (macrosomia, neonatal jaundice) in patients with GDM.

Keywords

diabetes gestational diabetes LncRNA SNHG14 MiR-493-5p

Introduction

Gestational diabetes mellitus (GDM) is a metabolic disorder characterized by the onset or first appearance of abnormal glucose tolerance during normal pregnancy.¹ GDM is a common complication of pregnancy. The prevalence of GDM is 14% globally and is increasing every year.^2,3 Although blood glucose levels in patients with GDM usually normalize after delivery, these women are at a significantly higher risk of developing type 2 diabetes in the future. At the same time, their offspring face a higher risk of metabolic syndrome and insulin resistance.⁴ GDM presents multiple complications in mid to late pregnancy that can increase adverse pregnancy outcomes for the maternal or offspring. Studies have shown a relationship between gestational hyperglycemia and adverse pregnancy outcomes, leading to conditions such as hyperbilirubinemia, neonatal respiratory distress syndrome, neonatal hypoglycemia, macrosomia, and metabolic syndrome.⁵ Therefore, identifying risk factors for GDM is important to avoid further development of GDM and reduce the occurrence of adverse pregnancy outcomes.

Long non-coding RNAs (lncRNAs) are non-coding RNAs (ncRNAs) that contain more than 200 nucleotides.⁶ lncRNA can control gene expression by directly interacting with DNA and activating or suppressing the functions of enhancers or promoters.⁶ In diabetes mellitus, lncRNAs can influence the disease by regulating signaling pathways that are related to glucose homeostasis.⁷ Among all the lncRNAs, the lncRNA small nucleolar RNA host gene (SNHG) was reported to be related to glucose homeostasis.^8,9 LncRNA small nucleolar RNA host gene 1 (SNHG1) was associated with kidney injury in diabetic nephropathy mice.⁸ LncRNA small nucleolar RNA host gene 14 (SNHG14) was responsible for the progression of diabetic nephropathy by regulating the miR-30e-5p/SRY-Box Transcription Factor 4 (SOX4, a transcription factor that regulates embryonic development and cellular activities) axis.⁹ For lncRNA SNHG14, however, whether it contributes to the progression of GDM in pregnant women remains unknown.

MicroRNAs (miRNAs) are ncRNAs that contain an average of 22 nucleotides.¹⁰ MiRNA can regulate gene expression by binding to the mRNA 3′-untranslated regions (3′UTR).¹⁰ MiRNAs thus participate in numerous biological processes and regulate the development of disease.¹¹ In diabetes mellitus, miRNAs can control glucose homeostasis and insulin production processes by participating in pancreatic islet development and intracellular insulin signalling.¹² Although the role of miRNA miRNA-493-5p (miR-493-5p) in glucose homeostasis remains unknown, in GDM, miR-493-5p can regulate GDM progression by targeting Thrombospondin 1 (THBS1, an extracellular matrix protein related to insulin resistance).¹³

It has been proved that the regulatory effect of miRNA on gene expression can be altered by lncRNA.⁶ LncRNA can directly bind to miRNA target genes or act as miRNA sponges.⁶ Investigating if miR-493-5p is a target of lncRNA SNHG14 and its influence on the development and progression of GDM might be the key to exploring efficient early diagnosis methods for GDM.¹⁴

Therefore, to explore efficient early diagnosis methods of GDM and reduce the incidence of adverse pregnancy outcomes in GDM patients, this study investigated the expression characteristics of lncRNA SNHG14 and miR-493-5p and their relationship in pregnant women with GDM and further explored their influence on the progression of GDM and the occurrence of adverse pregnancy outcomes.

Materials and methods

Ethical statement

All subjects and family members signed an informed consent form before enrollment. The study protocol was approved by the Ethics Committee of author’s institution and strictly followed the principles of the Declaration of Helsinki.

Study subjects

In this study, the required sample size to evaluate the difference in the expression of lncRNA SNHG14 and miR-493-5p between GDM cases and healthy controls in the t-test was determined using G*Power 3.1.9.7. The following parameters were defined for the power analysis: medium effect size of d = 0.5, alpha of 0.05 and power (1 - beta) of 0.8. The calculation of the required sample size showed that 64 participants were needed in each group (total N = 128). Considering the sample sizes used in other related studies,^15,16 this research included 128 patients with GDM admitted to our hospital between 2021 and 2023 as the study group. Additionally, 125 healthy pregnant women who underwent routine medical checkups at the hospital were selected to serve the control group. The GDM group and control group were determined when women were screened for GDM by doing oral glucose tolerance tests in mid-pregnancy (24–28 weeks). The age and gestation period of pregnant women in the healthy group were matched with GDM patients.

Inclusion criteria: (1) regular labor and delivery examination; (2) oral glucose tolerance test in mid-pregnancy (24–28 weeks, fasting blood glucose ≥5.1 mmol/L or 1 h after taking glucose blood glucose ≥10.0 mmol/L or 2 h after taking glucose blood glucose ≥8.5 mmol/L); (3) sound function of heart, liver, lungs, kidneys and other important organs.

Exclusion Criteria: (1) Previous diagnosis of diabetes mellitus or family history of diabetes mellitus; (2) Twin or multiple pregnancies; (3) Spontaneous miscarriage during the follow-up period; (4) Abnormal development of the fetus; (5) Incomplete clinical data; (6) Serious acute or chronic diseases, such as abnormalities of liver function, renal function, abnormalities of the thyroid gland, respiratory diseases, autoimmune diseases, hematologic or tumor-related diseases; (7) Serious acute or chronic diseases, such as abnormalities of liver function, renal function, abnormalities of the thyroid gland, respiratory diseases, autoimmune diseases, blood system or tumor-related diseases; (8) stressful injuries, such as surgery, trauma, etc.

Clinical samples collection

Venous blood samples were collected when pregnant women were screened for GDM, which was during 24 to 28 weeks of pregnancy of women. Before collecting the venous blood samples, both patients and healthy controls fasted for 12 h. Subsequently, venous blood samples of 5 mL were collected at 1 h and 2 h postprandial. The collected specimens were centrifuged and supernatant was taken, centrifuged at 4°C for 15 min at a rotating speed of 3000 g, and stored in a refrigerator at −80°C. The blood was collected on the same day.

Blood glucose testing and observation indicators

Patients’ blood glucose levels were determined by the hexokinase method. A fully automated biochemical analyzer AU5811 provided by Beckman Coulter Systems, Germany was used for the test. Neonatal weight and incidence of prematurity, asphyxia and pathologic jaundice were recorded.

Real time PCR

Detection of relative expression of lncRNA SNHG14 and miR-493-5p in serum. Total RNA was extracted from serum using an RNA extraction kit and reverse transcribed into cDNA using a reverse transcription kit. 20 μl of the Polymerase Chain Reaction (PCR) system was configured according to the instructions of the SYBR Pre-mix Ex Taq Ⅱ kit (Takara, Japan). The relative expression levels of lncRNA SNHG14 and miR-493-5p were sequentially detected in the sera of all study subjects using a fluorescence quantitative PCR instrument. The 2^−ΔΔCt method was calculated using GAPDH as an internal reference.

Cell culture

293T cell was purchased from the cell bank of the Typical Culture Preservation Committee of the Chinese Academy of Sciences. The cell lines were cultured in vitro in the minimum essential medium (MEM) containing 10% fetal bovine serum (FBS), 10 m/L streptomycin, and 10 m/L penicillin. The medium was incubated in an incubator at 37°C with 5% CO₂. The culture medium was changed every 2 days, and the cells were passaged at a 1:2 ratio approximately every 3 days. When the cell density reached 70%–90%, the cells were digested with trypsin containing 0.25% ethylene diamine tetraacetic acid (EDTA) to remove the wall, and the cells were cultured enough for a certain number and then frozen for storage.

Dual luciferase report

The binding sites of lncRNA SNHG14 and miR-493-5p were predicted using the online database ENCORI. Wild-type (WT) and mutant (MUT) lncRNA SNHG14 sequences containing the miR-493-5p binding site were ligated into the pmir- GLO dual luciferase reporter vector to obtain recombinant plasmids WT-lncRNA SNHG14 and MUT-lncRNA SNHG14. miR-493-5p mimic, miR-493-5p inhibitor and negative controls (mimic NC, inhibitor NC) were provided by RiboBio, Guangzhou, China. The cells were transfected into 293T cells using lipofectamine 2000 transfection reagent (Thermo, USA). There were 8 groups: (1) WT - lncRNA SNHG14 + mimic NC; (2) WT - lncRNA SNHG14 + miR-493-5p mimic; (3) WT - lncRNA SNHG14 + inhibitor NC; (4) WT - lncRNA SNHG14 + miR-493-5p inhibitor; (5) MUT - lncRNA SNHG14 + mimic NC (6) MUT - lncRNA SNHG14 + miR-493-5p mimic; (7) MUT - lncRNA SNHG14 + inhibitor NC; and (8) MUT - lncRNA SNHG14 + miR-493-5p inhibitor. 3 replicate wells were set up for each group. The medium was changed after 6 h of transfection and the culture was continued. The medium was aspirated after 48 h of transfection, and Renilla luciferase (Beyotime, China) assay was performed according to the instructions.

Data analysis

SPSS 23.0 was used to analyze the experimental data. Measurement data were expressed using mean ± standard deviation (xˉ ± s). Data significance between groups was analyzed using two-way ANOVA and two-by-two comparisons. Count data were expressed using examples and the χ2 test was used. The diagnostic value of lncRNA SNHG14 and miR-493-5p in GDM was evaluated using subject operating characteristic (ROC) curves. Logistic regression analysis was used to evaluate whether lncRNA SNHG14 and miR-493-5p were independent factors for the occurrence of GDM. Pearson’s correlation coefficient was used to determine the correlation between lncRNA SNHG14 and miR-493-5p. P < 0.05 was considered as statistically significant difference.

Results

Comparison of baseline data of the enrolled subjects

Clinical baseline indicators of the subjects were analyzed during the study. The mean age of 128 GDM patients included was 32.04 ± 3.92 years and gestational week was 37.87 ± 1.98 weeks. GDM patients with a history of alcohol consumption and smoking accounted for 30.47% and 32.03% of all GDM patients. In the same period, 125 women with normal pregnancies who had medical checkups in our hospital were selected as healthy controls, with a mean age of 31.37 ± 4.21 years and a gestational week of 38.30 ± 1.73 weeks. Pregnant women with a history of alcohol consumption and smoking in the healthy control group were also counted as 34.80% and 27.20%, respectively. There was no significant difference in age, body mass index (BMI), total gestational week, systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting blood glucose (FBG), history of alcohol consumption and smoking history between the control group and the group of patients with GDM (P > 0.050). Fasting blood glucose in the group of patients with GDM was 5.30 ± 0.11 mmol/L, which was significantly higher than that of the healthy pregnant women (4.53 ± 0.32 mmol/L, P < 0.0001). The post-prandial blood glucose and post-prandial 2-h blood glucose in the group of patients with GDM were 5.30 ± 0.11 mmol/L. 1 h blood glucose and postprandial 2 h blood glucose were also significantly higher than those of healthy controls (P < 0.0001, Table 1).

Table 1.

General information of the enroll participants.

Parameters	Controls group (n = 125)	GDM group (n = 128)	P values
Age (years)	31.37 ± 4.21	32.04 ± 3.92	0.191
BMI (kg/m²)	22.91 ± 3.21	22.56 ± 3.00	0.374
Gestation (weeks)	38.30 ± 1.73	37.87 ± 1.98	0.072
FBG (mmol/L)	4.53 ± 0.32	5.30 ± 0.11	0.000
1 h	6.28 ± 0.22	10.22 ± 0.31	0.000
2 h	5.40 ± 0.43	8.30 ± 0.21	0.000
SBP (mmHg)	114.90 ± 8.53	115.22 ± 9.10	0.777
DBP (mmHg)	72.18 ± 6.86	72.40 ± 6.57	0.800
Drinking history (n/%)			0.314
Yes	31 (24.80%)	39 (30.47%)
No	94 (75.20%)	89 (69.53%)
Smoking history (n/%)			0.400
Yes	34 (27.20%)	41 (32.03%)
No	91 (72.80%)	87 (67.97%)

Note: BMI: body mass index; FBG: fasting blood glucose; 1 h: 1-h postprandial blood glucose; 2 h: 2-h postprandial blood glucose; SBP: systolic blood pressure; DBP: diastolic blood pressure.

Prediction of target binding sites of lncRNA SNHG14, miR-493-5p and dual luciferase activity results

The targeting sites of lncRNA SNHG14 and miR-493-5p were predicted using the ENCORI database (Figure 1A). Co-transfection of WT-lncRNA SNHG14 and miR-493-5p mimic group showed a significant decrease in relative luciferase activity (P < 0.001). The relative luciferase activity of the co-transfected WT-lncRNA SNHG14 and miR-493-5p inhibitor groups increased significantly (P < 0.001). There was no significant difference in the relative luciferase activity of the MUT-lncRNA SNHG14 group (P > 0.050, Figure 1B).

Figure 1.

Binding of lncRNA SNHG14 to miR-493-5p. (A) Bioinformatics prediction of the binding site of lncRNA SNHG14 with miR-493-5p; (B) relative luciferase activity results of the cells in each group; (C) expression level of lncRNA SNHG14 in the serum of the subjects; (D) expression level of miR-493-5p in the serum of the subjects; (E) lncRNA SNHG14 correlation analysis with miR-493-5p. **P < 0.001.

Correlation of lncRNA SNHG14 and miR-493-5p in subjects

In GDM patients, the expression levels of lncRNA SNHG14 were significantly higher compared with the healthy group (P < 0.001, Figure 1C). While the expression level of miR-493-5p was significantly lower in GDM patients (Figure 1D, P < 0.001). Analysis revealed a negative correlation between lncRNA SNHG14 and miR-493-5p (r = −0.803, 95% CI = −0.857 to −0.731, P < 0.0001, Figure 1E).

Independent risk factors for the development of GDM predicted by logistics

Binary logistic regression analysis was performed for age, BMI, gestational week, SBP, DBP, history of alcohol consumption, history of smoking, and expression levels of lncRNA SNHG14 and miR-493-5p. The results showed that the expression levels of lncRNA SNHG14 (OR = 11.866, 95% CI = 5.942–23.698, P < 0.0001) and miR-493-5p (OR = 0.135, 95% CI = 0.068–0.269, P < 0.0001) were significantly associated with the occurrence of GDM (Table 2).

Table 2.

Independent influences of logistics in predicting the development of gestational diabetes mellitus.

Parameters	P values	Odds ratio (95% CI)
Age (years)	0.379	1.407 (0.658–3.011)
BMI (kg/m²)	0.469	1.287 (0.650–2.550)
Gestation (weeks)	0.218	1.537 (0.775–3.048)
SBP (mmHg)	0.750	1.117 (0.566–2.206)
DBP (mmHg)	0.640	1.176 (0.595–2.325)
Drinking history	0.680	1.156 (0.580–2.304)
Smoking history	0.778	1.117 (0.518–2.409)
lncRNA SNHG14	0.000	11.866 (5.942–23.698)
miRNA-493-5p	0.000	0.135 (0.068–0.269)

Correlation between blood glucose and lncRNA SNHG14, miR-493-5p

Serum lncRNA SNHG14 was positively correlated with fasting blood glucose, 1-h postprandial blood glucose and 2-h postprandial blood glucose levels in GDM patients (r = 0.614, P < 0.001; r = 0.769, P < 0.001; r = 0.739, P < 0.001, respectively). In addition, serum miR-493-5p was negatively correlated with fasting glucose, 1-h postprandial glucose and 2-h postprandial glucose levels in GDM patients (r = −0.519, P < 0.001; r = −0.633, P < 0.001; r = −0.566, P < 0.001, respectively, Table 3).

Table 3.

Correlation analysis of lncRNA SNHG14, miR-493-5p and blood glucose in GDM patients.

Parameters	lncRNA SNHG14		miR-493-5p
Parameters	r	P	r	P
FBG (mmol/L)	0.614	<0.001	−0.519	<0.001
1 h	0.769	<0.001	−0.633	<0.001
2 h	0.739	<0.001	−0.566	<0.001

Diagnostic value of serum lncRNA SNHG14 and miR-493-5p for GDM

The results showed that lncRNA SNHG14 had significant diagnostic value in distinguishing healthy pregnant women from GDM patients, with an AUC of 0.898 (95% CI = 0.861–0.934). The sensitivity and specificity were 0.852 and 0.776, respectively. MiR-493-5p, moreover, had significant diagnostic value in distinguishing healthy pregnant women from GDM patients. Its AUC was 0.872 (95% CI = 0.831–0.913). The sensitivity and specificity were 0.766 and 0.784, respectively. Finally, the ROC curve of lncRNA SNHG14 combined with miR-493-5p for diagnosing GDM was plotted. The AUC for the combined diagnosis was 0.948 (95% CI = 0.921–0.974). Its sensitivity and specificity were 0.883 and 0.904, respectively (Figure 2). The lncRNA SNHG14 combined with miR-493-5p has a higher AUC value for diagnosing GDM, so it has a higher diagnostic value.

Figure 2.

ROC curves analyzing the diagnostic value of lncRNA SNHG14 with miR-493-5p in GDM patients.

Relationship between serum lncRNA SNHG14, miR-493-5p and pregnancy outcome in GDM patients

Based on the average expression levels of serum lncRNA SNHG14 and miR-493-5p in GDM patients, patients were divided into high lncRNA SNHG14 expression group and low lncRNA SNHG14 expression group, and high miR-493-5p expression group and low miR-493-5p expression group. The relationship between the expression levels of lncRNA SNHG14 and miR-493-5p and pregnancy outcomes in GDM patients was analyzed. The results revealed that the expression level of lncRNA SNHG14 was significantly associated with neonatal weight, and neonatal jaundice (P < 0.001). In addition, the expression level of miR-493-5p was also significantly associated with neonatal jaundice (P < 0.001, Table 4).

Table 4.

Relationship between serum lncRNA SNHG14, miR-493-5p expression and neonatal prognosis in pregnant women with GDM.

Parameters	n	lncRNA SNHG14		P	miR-493-5p		P
Parameters	n	High (n = 67)	Low (n = 61)	P	High (n = 62)	Low (n = 66)	P
Neonatal weight				<0.001			0.071
≤4 kg	85	35	50		46	39
>4 kg	43	32	11		16	7
Premature delivery				0.217			0.178
Yes	20	13	7		7	13
No	108	54	54		55	53
Jaundice				<0.001			<0.001
Yes	36	31	5		6	30
No	92	36	56		56	36
Asphyxia				0.794			0.279
Yes	7	4	3		2	5
No	121	63	58		60	61

Discussion

The pathogenesis of GDM is not fully understood, but elevated blood glucose due to insulin resistance and relative insulin secretion deficiency is one of the important features of GDM.^17,18 LncRNA SNHG14 is involved in various biological processes, such as regulation of neuronal apoptosis and inflammation, obesity-induced endoplasmic reticulum stress in adipocytes, osteogenesis of mesenchymal stem cells, and proliferation and epithelial-mesenchymal transition in cancer cells.^19–22 In this study, the upregulation of the expression of lncRNA SNHG14 was the promoting factor of GDM and lncRNA SNHG14 was an independent prognostic factor for GDM. In diabetes mellitus, lncRNA SNHG14 was reported to influence glucose homeostasis and was responsible for the progression of diabetic nephropathy.⁹ This suggests that lncRNA SNHG14 contributes to the development of GDM in pregnant women. In recent years, the potential of blood-derived lncRNAs as early diagnostic targets for diseases is emerging as a clinical research hotspot.²³ In GDM, testing the expression level of lncRNA SNHG14 in the serum of pregnant women might be an efficient method to early diagnose the disease. Pregnant women with relatively high lncRNA SNHG14 expression levels have the risk of developing GDM and need early intervention for the disease. This study provides important information for developing early diagnosis and prevention methods of GDM in pregnant women.

LncRNAs could influence disease progression by targeting miRNA.^24,25 This study thus investigated the association between lncRNA SNHG14 and miR-493-5p and the effect of their interaction on GDM. The results showed that lncRNA SNHG14 could downregulate the expression of miR-493-5p. The downregulation of miR-493-5p was an independent prognostic factor for GDM and it could promote the development of the disease. Interestingly, the interaction between lncRNA SNHG14 and miR-493-5p had the highest AUC values in distinguishing healthy pregnant women from GDM patients. It was reported that the expression levels of miR-493-5p were significantly lower in GDM patients and it could influence GDM progression by regulating the expression of insulin resistance related genes.¹³ The results illustrated that miR-493-5p mediated the influence of lncRNA SNHG14 on GDM. Testing if there are upregulation of lncRNA SNHG14 and downregulation of miR-493-5p in the serum of pregnant women could be a useful method for diagnosing GDM in early pregnancy of women. Real-time monitoring of maternal lncRNA SNHG14 and miR-493-5p levels and timely intervention can effectively reduce the risk of GDM. This study proved the high diagnostic value of lncRNA SNHG14 and miR-493-5p dysregulation, and the results would contribute to reducing the risk of getting GDM for pregnant women.

It was also shown that lncRNA SNHG14 upregulation and miR-493-5p downregulation were associated with adverse pregnancy outcomes of GDM patients including a high incidence of macrosomia and neonatal jaundice. When insulin from GDM patients cannot pass through the placenta, it can stimulate fetal pancreatic β-cells to proliferate and secrete a large amount of insulin, which further activates the amino acid transferase system and promotes the synthesis of fats and proteins, resulting in the accumulation of fetal fat, which ultimately leads to the occurrence of macrosomia (newborns with a birth mass ≥4 kg at any gestational week).²⁶ Pregnant women with abnormally high blood sugar levels during pregnancy will have newborns with some degree of jaundice.²⁷ This was mainly due to the destruction of neonatal erythrocytes and the inability of the immature liver to remove excess bilirubin.²⁸ The results demonstrated that miR-493-5p mediated the aggravated effect of lncRNA SNHG14 on GDM, which further led to bad pregnancy outcomes in the offspring. Therefore, lncRNA SNHG14 and miR-493-5p may also be biomarkers for adverse pregnancy outcomes in women. Testing the expression levels of lncRNA SNHG14 and miR-493-5p could be an efficient method for predicting adverse pregnancy outcomes in women. Furthermore, interventing the dysregulation of lncRNA SNHG14 and miR-493-5p might be a useful strategy for reducing the incidence of adverse pregnancy outcomes in women.

This study still has limitations. For instance, a previous study has reported that THBS1 can act as a target gene of miR-493-5p in GDM.¹³ In this study, however, whether lncRNA SNHG14/miR-493-5p/THBS1 was a regulatory pathway of GDM is still unclear. Moreover, we did not record the previous diets of women during sample collection and the influence of diets on the development of GDM remains unknown. Further research was needed to solve the limitations of this study.

Conclusion

In this study, we found that lncRNA SNHG14 in combination with miR-493-5p may be an early diagnostic marker of GDM, which may provide a reference basis for specifying early interventions in the clinic. LncRNA SNHG14 and miR-493-5p were associated with the occurrence of adverse pregnancy outcomes (macrosomia, neonatal jaundice) in patients with GDM.

Footnotes

ORCID iD

Meiqin Li

Statements and declarations

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

Conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

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Early diagnosis value of lncRNA SNHG14 combined with miR-493-5p in gestational diabetes mellitus and its correlation with pregnancy outcome

Abstract

Background

Methods

Results

Conclusion

Keywords

Introduction

Materials and methods

Ethical statement

Study subjects

Clinical samples collection

Blood glucose testing and observation indicators

Real time PCR

Cell culture

Dual luciferase report

Data analysis

Results

Comparison of baseline data of the enrolled subjects

Prediction of target binding sites of lncRNA SNHG14, miR-493-5p and dual luciferase activity results

Correlation of lncRNA SNHG14 and miR-493-5p in subjects

Independent risk factors for the development of GDM predicted by logistics

Correlation between blood glucose and lncRNA SNHG14, miR-493-5p

Diagnostic value of serum lncRNA SNHG14 and miR-493-5p for GDM

Relationship between serum lncRNA SNHG14, miR-493-5p and pregnancy outcome in GDM patients

Discussion

Conclusion

Footnotes

ORCID iD

Statements and declarations

Funding

Conflicting interests

References