RESUMO
The association between gut microbiota and development of Graves' disease (GD) remains unclear. This study aimed to profile the gut microbiota of 65 patients newly diagnosed with GD before and after treatment and 33 physical examination personnel via 16S rRNA sequencing. Significant differences in the gut microbiota composition were observed between the two groups, showing relative bacterial abundances of 1 class, 1 order, 5 families, and 14 genera. After treatment, the abundance of the significantly enriched biota in the GD group decreased considerably, whereas that of the previously decreased biota increased considerably. Further, interleukin-17 levels decreased significantly. The random forest method was used to identify 12 genera that can distinguish patients with GD from healthy controls. Our study revealed that the gut microbiota of patients with GD exhibit unique characteristics compared with that of healthy individuals, which may be related to an imbalance in the immune system and gut microbiota.
RESUMO
Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease. Advanced glycation end products (AGEs) negatively affect the liver and accelerate NAFLD progression; however, the underlying mechanisms remain unclear. The present study aimed to examine the effect and mechanism of dietary AGEs on the mouse liver using bioinformatics and in vivo experimental approaches. Gene expression datasets associated with NAFLD were obtained from the Gene Expression Omnibus and differentially expressed genes (DEGs) were identified using GEO2R. Functional enrichment analyses were performed using the Database for Annotation, Visualization and Integrated Discovery and a proteinprotein interaction network for the DEGs was constructed using the Search Tool for the Retrieval of Interacting Genes database. MCODE, a Cytoscape plugin, was subsequently used to identify the most significant module. The key genes involved were verified in a dietary AGEinduced nonalcoholic steatohepatitis (NASH) mouse model using reverse transcriptionquantitative PCR (RTqPCR). The 462 DEGs associated with NAFLD in the two datasets, of which 34 overlapping genes were found in two microarray datasets. Functional analysis demonstrated that the 34 DEGs were enriched in the 'PPAR signaling pathway', 'central carbon metabolism in cancer', and 'cell adhesion molecules (CAMs)'. Moreover, four hub genes (cell deathinducing DFFAlike effector a, cell deathinducing DFFAlike effector c, fatty acidbinding protein 4 and perilipin 4) were identified from a proteinprotein interaction network and were verified using RTqPCR in a mouse model of NASH. The results suggested that AGEs and their receptor axis may be involved in NAFLD onset and/or progression. This integrative analysis identified candidate genes and pathways in NAFLD, as well as DEGs and hub genes related to NAFLD progression in silico and in vivo.