Chronic ethanol exposure also led to an overall downward shift in the expression of Wnt 1, Fzd3, Lef1, Bcl9, Wisp 1, Sfrp5, and Wif1. The expression of Ccnd1, a major regulator of the

cell cycle, was elevated in the control group at 24 hours. However, GSK2126458 ethanol treatment caused a delayed response and peak expression occurred at 72 hours post-PH. Treatment with PPARδ agonist rescued the ethanol-induced depression of Wnt gene expression for genes including Wnt1, Wnt7a, Fzd3, Lef-1, Tcf7l2, Bcl9, Ccnd1, Axin2, Wif1, and Sfrp2. Conclusions: These observations demonstrate that long-term ethanol consumption inhibits Wnt signaling, leading to an impairment of liver regeneration. Treatment with PPARδ agonist ameliorated this effect, suggesting that improvement of liver function in chronic ALD requires

the restoration of Wnt signaling in addition to insulin/IGF signaling. Disclosures: The following people have nothing to disclose: Chelsea Q. Xu, Suzanne M. de la Monte, Jack R. Wands, Miran Kim Using selected-ion flow-tube mass spectrometry (SIFT-MS), precise identification of trace gases in human breath can be achieved. Aim: To determine whether concentration of volatile compounds in breath correlates with diagnosis and severity of liver disease in pts with alcoholic hepatitis (AH). Methods: We prospectively recruited pts with liver disease into two groups: liver cirrhosis with AH (N=40) and liver cirrhosis with acute decompensation (AD) from find more etiologies other than alcohol (N=40). A healthy control group without liver disease was identified (N=43). Using Small molecule library screening SIFT-MS, precise identification of volatile compounds in breath

in parts per billion ranges was achieved in fasting state. Results: Of 14 pre-selected breath compounds, we identified 6 compounds that were elevated in pts with liver disease compared to healthy control. Those include 2-propanol, acetaldehyde, acetone, ethanol, pentane and trimethylamine (TMA). The levels of TMA, acetone and pentane, in particular, in breath were remarkably higher in pts with AH compared to those with AD and to healthy volunteer (p<0.001). Using ROC curve, we developed model for diagnosis of AH that included breath levels of TMA, Acetone and Pentane (TAP model). TAP provided excellent prediction accuracy for diagnosis of AH (AUC=0.93) with 97% sensitivity and 72% specificity for TAP score of 28. The levels of breath TMA moderately correlated with severity of AH as presented by MELD score [rho (95%CI); 0.38 (0.07, 0.69),p=0.018]. Isoprene and ethanol in breath were associated with survival in AH. Conclusion: Breathprint may provide non-invasive method for diagnosis of AH and may provide independent prognostic value in patients with AH. Background: Sestrins (Sesns) are a small family of stress-sensitive genes that control lipid metabolism. Chronic alcohol feeding leads to the alteration in lipogenic genes; which are under the regulation of Sesns.