Helicobacter pylori infection aggravates diet-induced nonalcoholic fatty liver in mice

Previous epidemiological studies have suggested a link between Helicobacter pylori (H. pylori) infection and nonalcoholic fatty liver disease (NAFLD), yet animal studies are lacking to elucidate this association. In this study, we evaluated the potential effects of H. pylori infection on NAFLD in mice.

We first established two strains of H. pylori infected mice model with either chow diet or high fat diet (HFD). The body and liver weight, blood glucose, serum transaminases and lipid levels and markers of hepatic inflammation were measured. Histological analyses were also performed on liver tissue. Expressions of fat synthesis genes as well as insulin signaling proteins were also determined.

After 24 weeks of treatment, the abdominal circumference, fasting blood glucose, low-density cholesterol and alanine transaminase were significantly increased in HFD feeding mice infected with H. pylori SS1 compared to HFD controls. Moreover, HFD fed mice infected with H. pylori SS1 showed significantly more liver steatosis. H. pylori SS1 infection inhibited phosphorylation of IRS1 and Akt and trended to increase the expression of IL-1β and TNF-α in the liver.

H. pylori infection is associated with NAFLD in C57BL/6 mice which depends on the bacterial strain and diet structure. The infection of H. pylori SS1 instead of NCTC11637 in combination with HFD induced more severe liver steatosis. H. pylori infection may play a role in NAFLD development and further studies are needed to determine whether H. pylori eradication can improve NAFLD risk.