Abstract
Objective: The incidence of Hashimoto’s thyroiditis (HT) in patients with metabolically unhealthy obesity (MUO) is generally higher than that in normal-weight individuals. However, the relationship among obesity, HT, and hypothyroidism remains unclear. Subjects and Methods: We searched the National Center for Biotechnology Information database and analyzed the abnormal expression of miRNAs in patients with MUO. The datasets GSE169290 and GSE138198 were selected as the objects of this data analysis. Using the MirPath tool on the DIANA TOOLS website, the KEGG pathway enrichment results were used for further analysis and explored the differential expression of pathways in patients with HT. Results: Four KEGG pathways were identified: “prion diseases (hsa05020),” “ECM-receptor interaction (hsa04512),” “mucin-type O-glycan biosynthesis (hsa00512),” and “cell adhesion molecules (hsa04514).” Sixteen differential genes were obtained, among which GALNT15 ranked the first, GALNT12 ranked the eighth, and GALNT8 ranked the 13th. GALNT15, GALNT12, and GALNT8 in the “mucin-type O-glycan biosynthesis” pathway are significantly lower in HT patients, which may be a key factor in the pathogenesis of HT. Conclusions: Decreased expression of O-GalNAc glycosylation in patients with MUO may increase the incidence of HT, which may become an important mechanism of HT in patients with obesity and is worthy of further exploration in future.
Published Version
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