Downregulation of mRNAs Encoding Keratin-Associated Proteins in the Tongue of Mice Fed a High-Fat Diet

Abstract

Although studies have indicated that there are associations between oral health and systemic diseases, the mechanisms linking these, particularly at the molecular level, remain largely unclear. We aimed to shed light on this issue by applying microarray analysis to survey gene expression in the tongue and liver of mice with fatty liver induced by feeding on a high-fat diet (HFD), as a model of metabolic syndrome. Here, C57BL/6 male mice were fed an HFD or a control diet for 24 weeks, with the samples obtained from them being subjected to analyses including with one-colored DNA array tips containing 23,475 genes. The results revealed 57 differentially expressed genes (DEGs) in liver and 21 in tongue. Among these 21 tongue-related DEGs, five Krtap (4-13, 5-2, 5-4, 9-1, and 13) genes exhibited significantly suppressed expression in the HFD group, while expression of the 21Krtap family genes analyzed as a single entity was also significantly suppressed. However, no histological changes were found in tongue, despite these 21 genes having differential expression there. Although the Krtap subfamily of keratins is mainly known as component proteins of hair follicles, little has been revealed about its functional diversity besides roles acting in support of keratins. Despite research in this field still being in its infancy, this study shows that Krtap downregulation in mice with fatty liver may be associated with structural frailty of tongue epithelium or even oral carcinogenesis. This work deepens our understanding of how an HFD can potentially affect the tongue, and opens up new avenues for exploring the connections between oral and systemic diseases and pursuing effective approaches to combating metabolic syndrome.