Abstract
Many risk factors related to the development of non-alcoholic fatty liver disease (NAFLD) have been proposed, including the most well-known of diabetes and obesity as well as periodontitis. As periodontal pathogenic bacteria produce endotoxins, periodontal treatment can result in endotoxemia. The aim of this study was to investigate the effects of intravenous, sonicated Porphyromonas gingivalis (Pg) injection on glucose/lipid metabolism, liver steatosis, and gut microbiota in mice. Endotoxemia was induced in C57BL/6J mice (8 weeks old) by intravenous injection of sonicated Pg; Pg was deactivated but its endotoxin remained. The mice were fed a high-fat diet and administered sonicated Pg (HFPg) or saline (HFco) injections for 12 weeks. Liver steatosis, glucose metabolism, and gene expression in the liver were evaluated. 16S rRNA gene sequencing with metagenome prediction was performed on the gut microbiota. Compared to HFco mice, HFPg mice exhibited impaired glucose tolerance and insulin resistance along with increased liver steatosis. Liver microarray analysis demonstrated that 1278 genes were differentially expressed between HFco and HFPg mice. Gene set enrichment analysis showed that fatty acid metabolism, hypoxia, and TNFα signaling via NFκB gene sets were enriched in HFPg mice. Although sonicated Pg did not directly reach the gut, it changed the gut microbiota and decreased bacterial diversity in HFPg mice. Metagenome prediction in the gut microbiota showed enriched citrate cycle and carbon fixation pathways in prokaryotes. Overall, intravenous injection of sonicated Pg caused impaired glucose tolerance, insulin resistance, and liver steatosis in mice fed high-fat diets. Thus, blood infusion of Pg contributes to NAFLD and alters the gut microbiota.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome (Jensen et al, 2018)
We reported that swallowing of the periodontal pathogenic bacteria Aggregatibacter actinomycetemcomitans changes the gut microbiota and is a possible risk factor for NAFLD (Komazaki et al, 2017)
In the present study, we investigated the effect of intravenously injected sonicated P. gingivalis on glucose/lipid metabolism and liver steatosis
Summary
Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome (Jensen et al, 2018). Periodontal bacteria, including Porphyromonas gingivalis, produce various virulence factors such as LPS, fimbriae, and enzymes, which can lead to inflammation in periodontal tissues (Kolenbrander et al, 2002). Yoneda et al (2012) first reported that infection with P. gingivalis may be a risk factor for the development and progression of NAFLD. We reported that swallowing of the periodontal pathogenic bacteria Aggregatibacter actinomycetemcomitans changes the gut microbiota and is a possible risk factor for NAFLD (Komazaki et al, 2017). In ligature-induced periodontitis, periodontal bacteria naturally accumulate around the teeth, and increase liver steatosis in rats (Kuraji et al, 2016; Pessoa et al, 2018). In ligature-induced periodontitis, periodontal bacteria naturally accumulate around the teeth, and increase liver steatosis in rats (Kuraji et al, 2016; Pessoa et al, 2018). Imajo et al (2012) reported that the response to low-dose LPS was enhanced by liver steatosisinduced high-fat diet feeding, and additional low-dose LPS administration led to liver injury and severe hepatic fibrosis in mice
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