Due to high cost-to-society of alcoholism and and the significant morbidity of alcoholic liver disease (ALD), our team has focused on mouse models which can be used to study the mechanism of action of Ppar proteins which may protect liver against alcohol-induced damage. Our main focus has been in studying the metabolic changes in urine, serum, and liver tissue of mice on chronic alcohol diet. For instance, the protective role of proliferator-activated receptor-β/δ (PPARβ/δ) against ALD has been extensively studied in wild-type and Pparβ/δ-null mice has an important role in preventing alcoholic liver disease (ALD). We have employed sensitive and accurate time of flight mass spectrometers (TOF-MS) coupled with ultra performance liquid chromatography (UPLC) along with biochemical assays and liver tissue histopathology supplied by our collaborators at PSU to identify key metabolites which may shed light on the role of PPARβ/δ. Our results collectively have shown a ca higher lipid accumulation in the liver of knockout mice which may point to the role of PPARβ/δ in inhibiting alcohol-induced hepatic lipogenesis, modulating amino acid metabolism, and altering pyridoxal kinase activity. The results of this study have been published in Toxicology, 2013.