Fatty liver disease caused by high alcohol-producing Klebsiella pneumoniae

To further explore the overall development and progression of hepatic steatosis induced by HiAlc Kpn, we examined liver transcriptional profiles derived HiAlc Kpn-fed, pair-fed, or ethanol-fed mice for the 4th, 6th and 8th week post gavage. The liver gene expressions in mice both with HiAlc Kpn-fed and ethanol-fed have been showed large diversities to pair-fed mice. These results clearly illustrated a process of chronic liver injury, which is consistent with previous “two-hits” insulin hypothesis, and suggested that endogenous ethanol produced by HiAlc Kpn play important roles in the steatohepatitis, as well as alcohol intake. Kpn-fed, pair-fed (negative control), or ethanol-fed induced gene expression in mice was measured at 4th, 6th and 8th week post gavage.