Hepatic CIDEC mRNA levels were correlated positively with hepatic

Hepatic CIDEC mRNA levels were correlated positively with hepatic steatosis, the disease severity (MELD and ABIC score, HVPG), and mortality in AH patients. In conclusion, this long-term chronic plus binge ethanol feeding model partially

simulates the histo-logical and molecular features of human AH. FSP27/CIDE-C plays a critical role in promoting steatosis and hepatocellular damage in long-term chronic plus binge ethanol-fed mice and in human AH. Disclosures: Jim Lu – Employment: GoPath Pathology Associates, SC; Independent Contractor: GoPath Laboratories LLC; Management Position: GoPath Global LLC Ramon Bataller – Advisory Committees or Review Panels: Sandhill; Consulting: VTI The following people have nothing to disclose: Ming-Jiang Xu, Yan Cai, Jose T. Altamirano, Binxia Chang, Hua Wang, Adeline Bertola, Gemma Odena, Kimi-hiko Talazoparib cell line RAD001 order Matsusue, Shioko Kimura, Frank J. Gonzalez, Bin Gao BACKGROUND: Alcoholic and nonalcoholic fatty liver disease (ALD and NAFLD) commonly occur

in overweight or obese subjects (OW-OB). The impact of etiology on the intestinal micro-biome in the background of OW-OB is not known. AIMS: To compare the intestinal microbiome of OW-OB ALD to healthy controls and subjects with nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH), and their relationship to markers of liver injury. METHODS: Fecal 16S pyrosequenc-ing was performed on subjects with ALD, NAFL, NASH or weight-matched controls without fatty liver disease. The abundance of microbiota were compared using partial least squares discriminant analysis, parametric and nonparametric multiple group testing. Multiple regression analyses were used to relate liver injury markers to microbiota. RESULTS: Ninety eight subjects enrolled in total (mean BMI in kg/m2) – control, n=21 (26.7±5.3), NAFL, n=25

(32.5±5.3), NASH, n=35 (34.2±4.1) and ALD, n=17 (31.9±9) were studied. Microbial abundance : (a) Increased in ALD: Phyla : Proteobacteria (p< 0.008), Class: Firmicutes_Bacilli and Proteobacteria_Gammaproteobacteria (p< 0.01-0.0001), Order: Bifidobacteriales (p=0.01 vs. NAFL, 0.004 vs. NASH), Lactobacillales (p=0.02 vs. control and NASH), Enterobacteriales PtdIns(3,4)P2 (p=0.003 vs. control, p=0.0001 vs. NAFL and NASH), Family: Bifidobacteriaceae (p<0.01 both NAFL and NASH), Enterobacteriaceae (p=0.003 vs. control, p=0.0001 vs. NAFL and NASH), and Genus: Bifidobacterium (p=0.01 vs. NAFL, p=0.004 vs. NASH) and Escherichia/Shi-gella (p=0.008 vs. controls, p=0.016 vs. NAFL and p=0.009 vs. NASH). (b) Decreased in ALD: Phyla: Bacteroidetes (p=0.03 vs. NAFL, p=0.01 vs. NASH), Class: Bacteroidetes_Bacteroidia (p=0.03 vs. NAFL, p=0.01 vs. NASH) and Firmicutes_Clos-tridia (p=0.0023 vs. control, p=0.036 vs. NAFL and p=0.041 vs. NASH) (c) Changes in NAFLD: Only Actinobacteria had lower abundance in NASH vs. control (p=0.

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