Background <p>Recent studies have suggested that periodontitis affects non-alcoholic fatty liver disease (NAFLD). Until now, the underlying mechanisms have mainly been investigated in the context of diabetes, which is a risk factor for NAFLD. However, clinical research indicates that 80% of NAFLD patients do not have diabetes, with a complication rate of 40% even in advanced cases. In this study, we investigated whether periodontitis exacerbates NAFLD under non-diabetic conditions using a high-carbohydrate/high-fat diet (HCHFD).</p> Methods <p>We first developed non-diabetic NAFLD mice induced by an HCHFD and then analyzed the effect of ligature-induced periodontitis in an established NAFLD mouse model. Mice were fed a normal chow (NC), an HCHFD, or a high-fat diet (HFD), a commonly used diet in previous NAFLD studies for 6&#xa0;weeks.</p> Results <p>HCHFD induced hepatic steatosis without causing glucose intolerance or insulin resistance, whereas a HFD showed glucose intolerance accompanied by hepatic steatosis. Ligature-induced periodontitis facilitated HCD-induced steatosis and caused interlobular fibrosis in the liver.</p> Conclusion <p>A non-diabetic mouse model for NAFLD, closer to the clinical presentation than pre-existing mouse models, indicated that ligature-induced periodontitis exacerbated non-diabetic NAFLD, which accounts for the majority of the NAFLD population.</p>

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Ligature-induced periodontitis exacerbates high-carbohydrate/high-fat diet-induced fatty liver in mice under non-diabetic conditions

  • Misako Tari,
  • Mikihito Kajiya,
  • Tsuyoshi Fujita,
  • Kazuhisa Ouhara,
  • Tomoyuki Iwata,
  • Shinji Matsuda,
  • Hidemi Kurihara,
  • Noriyoshi Mizuno

摘要

Background

Recent studies have suggested that periodontitis affects non-alcoholic fatty liver disease (NAFLD). Until now, the underlying mechanisms have mainly been investigated in the context of diabetes, which is a risk factor for NAFLD. However, clinical research indicates that 80% of NAFLD patients do not have diabetes, with a complication rate of 40% even in advanced cases. In this study, we investigated whether periodontitis exacerbates NAFLD under non-diabetic conditions using a high-carbohydrate/high-fat diet (HCHFD).

Methods

We first developed non-diabetic NAFLD mice induced by an HCHFD and then analyzed the effect of ligature-induced periodontitis in an established NAFLD mouse model. Mice were fed a normal chow (NC), an HCHFD, or a high-fat diet (HFD), a commonly used diet in previous NAFLD studies for 6 weeks.

Results

HCHFD induced hepatic steatosis without causing glucose intolerance or insulin resistance, whereas a HFD showed glucose intolerance accompanied by hepatic steatosis. Ligature-induced periodontitis facilitated HCD-induced steatosis and caused interlobular fibrosis in the liver.

Conclusion

A non-diabetic mouse model for NAFLD, closer to the clinical presentation than pre-existing mouse models, indicated that ligature-induced periodontitis exacerbated non-diabetic NAFLD, which accounts for the majority of the NAFLD population.