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Journal of hepatology, ISSN 0168-8278, 2011, Volume 54, Issue 4, pp. 773 - 794
Numerous investigations have shown that mitochondrial dysfunction is a major mechanism of drug-induced liver injury, which involves the parent drug or a reactive metabolite generated through cytochromes P450... 
Gastroenterology and Hepatology | Drugs | Obesity | Oxidative stress | Mitochondria | Cell death | Lipids | Hepatotoxicity | Steatosis | TRIGLYCERIDE TRANSFER PROTEIN | DNA-POLYMERASE-GAMMA | PREGNANE X-RECEPTOR | PROLIFERATOR-ACTIVATED RECEPTOR | HEPATIC CYTOCHROME-P450 2E1 | ELEMENT-BINDING PROTEINS | FATTY-ACID OXIDATION | CONSTITUTIVE ANDROSTANE RECEPTOR | MANGANESE SUPEROXIDE-DISMUTASE | STRESS-RELATED PARAMETERS | GASTROENTEROLOGY & HEPATOLOGY | Carbohydrate Metabolism - drug effects | Reactive Oxygen Species - metabolism | Mitochondria, Liver - metabolism | Humans | Leptin - metabolism | Oxidative Phosphorylation - drug effects | Adipose Tissue - metabolism | Adiponectin - metabolism | Hepatitis C - complications | Cell Death - drug effects | Fatty Acids - metabolism | Chemical and Drug Induced Liver Injury - etiology | Diabetes Mellitus, Type 2 - complications | Genetic Predisposition to Disease | Fatty Liver - metabolism | Oxidation-Reduction | Obesity - complications | Insulin Resistance | Mitochondrial Membrane Transport Proteins - drug effects | Chemical and Drug Induced Liver Injury - genetics | Mitochondria, Liver - drug effects | Animals | Chemical and Drug Induced Liver Injury - metabolism | Models, Biological | Lipid Metabolism - drug effects | Alcoholic Intoxication - complications | Genome, Mitochondrial | Adipose Tissue - drug effects | Energy Metabolism - drug effects | Fatty Liver - etiology | Divalproex | Liver diseases | Thiols | Liver | Cytochrome P-450 | Mitochondrial DNA | Triglycerides | Stavudine | Permeability | Valproic acid | Fatty acids | Cells | Carnitine | Metabolites | Glutathione transferase | Acetaminophen | Physiological aspects | DNA polymerases | Health aspects | Zidovudine | Index Medicus | Reactive Oxygen Species | Fatty Acids | Adiponectin | Mitochondria, Liver | Life Sciences | Mitochondrial Membrane Transport Proteins | Cell Death | Diabetes Mellitus, Type 2 | Adipose Tissue | Alcoholic Intoxication | Hépatology and Gastroenterology | Oxidative Phosphorylation | Carbohydrate Metabolism | Lipid Metabolism | Drug-Induced Liver Injury | Fatty Liver | Human health and pathology | Energy Metabolism | Leptin | Hepatitis C
Journal Article
Journal of Gastroenterology and Hepatology, ISSN 0815-9319, 03/2009, Volume 24, Issue 3, pp. 443 - 452
... 3 activation, liver injury and liver pathology in mice fed a methionine and choline deficient (MCD) diet... 
mitochondria | methionine and choline deficiency | insulin‐like growth factor‐1 | TRAIL‐R killer/DR5 | TNF receptors | cell death pathways | p53 | Cell death pathways | TRAIL-R killer/DR5 | Methionine and choline deficiency | Mitochondria | Insulin-like growth factor-1 | P53 | HEPATOCYTE APOPTOSIS | ACIDS | DR5 | insulin-like growth factor-1 | NONALCOHOLIC STEATOHEPATITIS | LIVER-DISEASE | PATHOGENESIS | NECROSIS | TNF-ALPHA | LIGAND | GASTROENTEROLOGY & HEPATOLOGY | TRAIL-R killer | NF-KAPPA-B | HEPATIC STEATOSIS | Liver - pathology | Liver - enzymology | Fatty Liver - pathology | Mitochondria, Liver - metabolism | Caspase 3 - metabolism | Choline Deficiency - complications | Male | Alanine Transaminase - blood | Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism | Receptors, Tumor Necrosis Factor, Type I - metabolism | RNA, Messenger - metabolism | fas Receptor - metabolism | Tumor Suppressor Protein p53 - genetics | Time Factors | Receptors, Tumor Necrosis Factor, Type II - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Nutritional Status | Receptors, TNF-Related Apoptosis-Inducing Ligand - genetics | BH3 Interacting Domain Death Agonist Protein - metabolism | Disease Models, Animal | Methionine - deficiency | Receptors, Tumor Necrosis Factor - metabolism | Fatty Liver - metabolism | Mitochondria, Liver - pathology | Liver - metabolism | Mice, Inbred C57BL | Gene Expression Regulation | Tumor Suppressor Protein p53 - metabolism | Mitochondria, Liver - enzymology | Animals | Mice | bcl-X Protein - metabolism | Insulin-Like Growth Factor I - metabolism | Apoptosis | Fatty Liver - etiology | BH3 Interacting Domain Death Agonist Protein, metabolism | Receptors, Tumor Necrosis Factor, Type II, metabolism | Fatty Liver, pathology | Mitochondria, Liver, metabolism | Receptors, Tumor Necrosis Factor, metabolism | Cyclin-Dependent Kinase Inhibitor p21, metabolism | Insulin-Like Growth Factor I, metabolism | Caspase 3, metabolism | Antigens, CD95, metabolism | RNA, Messenger, metabolism | Tumor Suppressor Protein p53, metabolism | Methionine, deficiency | Choline Deficiency, complications | Tumor Suppressor Protein p53, genetics | bcl-X Protein, metabolism | Mitochondria, Liver, pathology | Liver, pathology | Alanine Transaminase, blood | Liver, metabolism | Fatty Liver, metabolism | Receptors, TNF-Related Apoptosis-Inducing Ligand, metabolism | Liver, enzymology | Fatty Liver, etiology | Mitochondria, Liver, enzymology | Receptors, Tumor Necrosis Factor, Type I, metabolism | Receptors, TNF-Related Apoptosis-Inducing Ligand, genetics | Messenger RNA | Choline | Methionine | Mitochondrial DNA | Tumor proteins | Peptide hormones | Growth factors
Journal Article
Acta Physiologica, ISSN 1748-1716, 05/2009, Volume 196, Issue 1, pp. 81 - 98
As the liver is central in the maintenance of glucose homeostasis and energy storage, knowledge of the physiology as well as physiopathology of hepatic energy metabolism is a prerequisite... 
hepatic glucose production | fatty liver | type 2 diabetes | AMP-activated protein kinase | liver | energy metabolism | AMP‐activated protein kinase | Type 2 diabetes | Energy metabolism | Fatty liver | Hepatic glucose production | Liver | PHYSIOLOGY | LIPID-METABOLISM | CREB COACTIVATOR TORC2 | ACETYL-COA CARBOXYLASE | MICE LACKING ADIPONECTIN | LIVER-DISEASE | ISOLATED RAT HEPATOCYTES | SKELETAL-MUSCLE | FATTY-ACID OXIDATION | INSULIN-RESISTANCE | ADIPOSE-TISSUE | AMP-Activated Protein Kinases - metabolism | Liver - enzymology | Hypoglycemic Agents - metabolism | Humans | Homeostasis | Protein Subunits - metabolism | Liver Cirrhosis - metabolism | Aminoimidazole Carboxamide - metabolism | Energy Metabolism - physiology | Protein Subunits - genetics | Liver Cirrhosis - drug therapy | Dyslipidemias - drug therapy | Ribonucleotides - metabolism | Fatty Liver - metabolism | Fatty Liver - physiopathology | Lipid Metabolism | Mitochondria - metabolism | AMP-Activated Protein Kinases - chemistry | Fatty Liver - drug therapy | Gluconeogenesis - physiology | Animals | Aminoimidazole Carboxamide - analogs & derivatives | Dyslipidemias - metabolism | Glucose - metabolism | Protein Conformation | Liver - cytology | Protein Subunits - chemistry | Liver Cirrhosis - physiopathology | AMP-Activated Protein Kinases - genetics | Dyslipidemias - physiopathology | Glucose metabolism | Enzymes | Liver diseases | Physiological aspects | Protein biosynthesis | Insulin resistance | Glucose | Protein kinases | Health aspects | Fatty acids | Dextrose | cytology | Protein Subunits | Dyslipidemias | AMP-Activated Protein Kinases | therapeutic | Hypoglycemic Agents | Aminoimidazole Carboxamide | Mitochondria | genetics | Gluconeogenesis | chemistry | drug therapy | physiology | Liver Cirrhosis | enzymology | Fatty Liver | physiopathology | Ribonucleotides | Energy Metabolism | analogs & derivatives | MP-activated protein kinase | metabolism
Journal Article
Drug Metabolism Reviews, ISSN 1097-9883, 2012, Volume 44, Issue 1, pp. 34 - 87
A frequent mechanism for drug-induced liver injury (DILI) is the formation of reactive metabolites that trigger hepatitis through direct toxicity or immune reactions... 
drug-induced liver injury | susceptibility | idiosyncrasy | liver | hepatotoxicity | mitochondria | mitochondrial DNA | mitochondrial permeability transition | mitochondrial dysfunction | Adverse drug reactions | hepatitis | steatosis | adverse drug reactions | PERMEABILITY TRANSITION PORE | COA DEHYDROGENASE-DEFICIENCY | ENDOPLASMIC-RETICULUM STRESS | HUMAN-IMMUNODEFICIENCY-VIRUS | ISOLATED RAT HEPATOCYTES | REVERSE-TRANSCRIPTASE INHIBITORS | HEPATITIS-C VIRUS | HEPATOCYTE PLASMA-MEMBRANE | FATTY-ACID OXIDATION | MANGANESE SUPEROXIDE-DISMUTASE | PHARMACOLOGY & PHARMACY | Liver - pathology | Fatty Liver - metabolism | Mitochondria, Liver - pathology | Reactive Oxygen Species - metabolism | Oxidation-Reduction | DNA, Mitochondrial - drug effects | Fatty Liver - pathology | Mitochondria, Liver - metabolism | Humans | Liver - metabolism | Mitochondrial Proteins - biosynthesis | Mitochondria, Liver - drug effects | Mitochondrial Proteins - drug effects | Pharmaceutical Preparations - metabolism | Chemical and Drug Induced Liver Injury - metabolism | Immune System - metabolism | Drug-Related Side Effects and Adverse Reactions | Mitochondria, Liver - ultrastructure | Cell Respiration - drug effects | Chemical and Drug Induced Liver Injury - pathology | DNA, Mitochondrial - biosynthesis | Fatty Liver - etiology | Index Medicus | Hépatology and Gastroenterology | Reactive Oxygen Species | Liver | DNA, Mitochondrial | Drug-Induced Liver Injury | Mitochondrial Proteins | Fatty Liver | Mitochondria, Liver | Life Sciences | Human health and pathology | Cell Respiration | Immune System | Pharmaceutical Preparations
Journal Article