ABSTRACT
The objective of this study was to evaluate the potential relationship between serum vaspin levels and gestational diabetes mellitus (GDM). The PubMed, EBSCO, Web of Science, the Cochrane Library, and the China National Knowledge Infrastructure (CNKI) database were searched for articles published before December 2022. The publication language was restricted to English and Chinese. A meta-analysis was conducted by combining all studies that met the inclusion and exclusion criteria. Twenty-two studies (1990 women with GDM and 1597 pregnant women without GDM) were ultimately included in this meta-analysis. The meta-analysis showed that the serum vaspin levels are significantly higher in GDM compared with the controls (standardized mean difference: 0.720, 95% confidence interval: 0.440-1.000, Z = 5.041, P < 0.001). Subgroup analyses by stage of pregnancy and body mass index showed results similar to the overall outcome. No publication bias was identified, and the sensitivity analysis confirmed the robustness of the final result. Our results show that the serum vaspin levels are significantly higher in GDM. These findings suggest that high vaspin concentration is closely related to GDM and the serum vaspin levels might be a potential biomarker to indicate risk of GDM, more randomized control trials comparing the expression levels of vaspin between early and standard diagnosis of GDM are needed to strengthen our findings.
Subject(s)
Diabetes, Gestational , Serpins , Female , Humans , Pregnancy , Biomarkers , China/epidemiology , Diabetes, Gestational/metabolism , Serpins/blood , Serpins/chemistryABSTRACT
Our previous studies have also demonstrated that AVP can significantly improve social interaction disorders and stereotypical behaviours in rats with VPA-induced autism model. To further explore the mechanisms of action of AVP, we compared the PFC transcriptome changes before and after AVP treatment in VPA-induced autism rat model. The autism model was induced by intraperitoneally injected with VPA at embryonic day 12.5 and randomly assigned to two groups: the VPA-induced autism model group and the AVP treatment group. The AVP treatment group were treated with intranasal AVP at postnatal day 21 and for 3 weeks. The gene expression levels and function changes on the prefrontal cortex were measured by RNA-seq and bioinformatics analysis at PND42 and the mRNA expression levels of synaptic and myelin development related genes were validated by qPCR. Our results confirmed that AVP could significantly improve synaptic and axon dysplasia and promote oligodendrocyte development in the prefrontal cortex in VPA-induced autism models by regulating multiple signalling pathways.
Subject(s)
Arginine Vasopressin , Autistic Disorder , Animals , Rats , Arginine Vasopressin/metabolism , Arginine Vasopressin/pharmacology , Autistic Disorder/drug therapy , Autistic Disorder/genetics , Autistic Disorder/chemically induced , Disease Models, Animal , Prefrontal Cortex/metabolism , Transcriptome/genetics , Valproic Acid/adverse effectsABSTRACT
Background: Some studies have shown that arginine vasopressin (AVP) can significantly improve the social interaction disorder of autism, but the mechanism remains unclear. Methods: Female Wistar rats were intraperitoneally injected with VPA or normal saline at embryonic day 12.5 to establish an autism model or normal control in their offspring. Male offspring prenatally exposed to VPA were randomly assigned to two groups: the VPA-induced autism model group and the AVP group. The rats in the AVP group were treated with intranasal AVP at postnatal day (PND) 21 and for 3 weeks. The VPA-induced autism model group was given the same dose of normal saline in the same way. Behavioral responses were evaluated in the open field and three-chambered social test apparatus; the expression levels of AVP in serum were detected by enzyme-linked immunosorbent assay kit, and the gene expression levels on the amygdala were measured by RNA-seq at PND42. Results: Intranasal administration of AVP can significantly improve the social interaction disorder and elevate the levels of AVP in serum. Transcriptome sequencing results showed that 518 differently expressed genes (DEGs) were identified in the VPA-induced autism model group compared with the control in this study. Gene Ontology biological process enrichment analysis of DEGs showed that the VPA-induced autism model group had significant nervous system developmental impairments compared with the normal group, particularly in gliogenesis, glial cell differentiation, and oligodendrocyte differentiation. Gene Set Enrichment Analysis (GSEA) enrichment analysis also showed that biological process of oligodendrocyte differentiation, axoneme assembly, and axon ensheathment were inhibited in the VPA-induced autism model group. Pathway enrichment analysis of DEGs between the control and VPA-induced autism model group showed that the PI3K/AKT and Wnt pathways were significantly dysregulated in the VPA-induced autism model group. Few DEGs were found when compared with the transcriptome between the VPA-induced autism model group and the AVP treatment group. GSEA enrichment analysis showed deficits in oligodendrocyte development and function were significantly improved after AVP treatment; the pathways were mainly enriched in the NOTCH, mitogen-activated protein kinase, and focal adhesion signaling pathways, but not in the PI3K/AKT and Wnt pathways. The expression patterns analysis also showed the same results. Conclusion: AVP can significantly improve the social interaction disorder of VPA-induced autism model, and AVP may target behavioral symptoms in autism by modulating the vasopressin pathways, rather than primary disease mechanisms.
