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Laboratory Investigation, ISSN 0023-6837, 05/2012, Volume 92, Issue 5, pp. 713 - 723
Non-alcoholic steatohepatitis (NASH) is typically associated with pro-apoptotic caspase activation. A potential role for pro-inflammatory caspases remains... 
Inflammasome | Inflammation | Caspases | Non-alcoholic fatty liver disease | Non-alcoholic steatohepatitis | Fibrosis | MEDICINE, RESEARCH & EXPERIMENTAL | POPULATION | APOPTOSIS | non-alcoholic fatty liver disease | MICE DEFICIENT | FATTY LIVER-DISEASE | INJURY | NONALCOHOLIC STEATOHEPATITIS | MODEL | PATHOLOGY | inflammation | inflammasome | fibrosis | caspases | HEPATIC STEATOSIS | non-alcoholic steatohepatitis | Tumor Necrosis Factor-alpha - metabolism | Liver - pathology | Clodronic Acid - pharmacology | Fatty Liver - pathology | Actins - metabolism | Caspase 3 - metabolism | Hepatic Stellate Cells - metabolism | Caspase 1 - metabolism | Choline Deficiency - complications | Hepatocytes - pathology | Hepatocytes - metabolism | Fatty Liver - chemically induced | LIM Domain Proteins - metabolism | Liver Cirrhosis - chemically induced | Inflammation - metabolism | Caspase 3 - blood | Interleukin-1beta - metabolism | Choline Deficiency - metabolism | Liver Cirrhosis - metabolism | Muscle Proteins - metabolism | Antigens, Differentiation - metabolism | Kupffer Cells - metabolism | Hepatic Stellate Cells - pathology | Methionine - deficiency | Collagen Type I - metabolism | Fatty Liver - metabolism | Liver - metabolism | Mice, Inbred C57BL | Nuclear Proteins - metabolism | Choline Deficiency - pathology | Kupffer Cells - drug effects | Mice, Knockout | Animals | Caspase 1 - genetics | Caspase 1 - deficiency | Liver Cirrhosis - pathology | Mice | Transforming Growth Factor beta - metabolism | Nonalcoholic fatty liver disease (NAFLD) | nonalcoholic steatohepatitis (NASH)
Journal Article
Nature, ISSN 0028-0836, 04/2011, Volume 472, Issue 7341, pp. 57 - 65
Metabolomics studies hold promise for the discovery of pathways linked to disease processes. Cardiovascular disease (CVD) represents the leading cause of death... 
CHLAMYDIA-PNEUMONIAE | TRIMETHYLAMINE-N-OXIDE | DNA METHYLATION | MULTIDISCIPLINARY SCIENCES | MURINE MACROPHAGES | MOUSE | GENE-EXPRESSION | ATHEROSCLEROSIS | MICE | CORONARY-HEART-DISEASE | MASS-SPECTROMETRY | Choline - metabolism | Dietary Fats - metabolism | Metabolomics | Liver - enzymology | Diet - adverse effects | Atherosclerosis - genetics | Betaine - metabolism | Humans | Phosphatidylcholines - administration & dosage | Phosphatidylcholines - metabolism | Choline - blood | Dietary Fats - pharmacology | Oxygenases - metabolism | Cardiovascular Diseases - blood | Female | Atherosclerosis - microbiology | Betaine - blood | Methylamines - pharmacology | Cardiovascular Diseases - diagnosis | Methylamines - metabolism | Receptors, Scavenger - metabolism | Biomarkers - metabolism | Phosphatidylcholines - blood | Cardiovascular Diseases - metabolism | Risk Assessment | Atherosclerosis - chemically induced | Mice, Inbred C57BL | Phosphatidylcholines - pharmacology | Gene Expression Regulation | Methylamines - blood | Gastrointestinal Tract - microbiology | Biomarkers - blood | Dietary Fats - blood | Atherosclerosis - metabolism | Gastrointestinal Tract - metabolism | Cardiovascular Diseases - microbiology | Macrophages - metabolism | Phenotype | Animals | Choline - administration & dosage | Choline - pharmacology | Germ-Free Life | Cholesterol, HDL - blood | Mice | Oxygenases - genetics | Lecithin | Microbiota (Symbiotic organisms) | Physiological aspects | Research | Cardiovascular diseases | Metabolism | Health aspects | Risk factors | Plasma | Nuclear magnetic resonance--NMR | Heart attacks | Pathogenesis | Lipids | Cardiovascular disease | Probiotics | Metabolites | Diet | Atherosclerosis | Bacteria | Insulin resistance | Mass spectrometry | atherosclerosis | intestinal microbiota | choline | diet | phospholipid | metabolomics
Journal Article
Annual Review of Medicine, ISSN 0066-4219, 02/2011, Volume 62, Issue 1, pp. 361 - 380
Novel, culture-independent, molecular and metagenomic techniques have provided new insight into the complex interactions between the mammalian host and gut... 
energy homeostasis | microbiome | TLR4 | gut flora | endotoxin | MEDICINE, RESEARCH & EXPERIMENTAL | CONJUGATED LINOLEIC-ACID | FATTY LIVER-DISEASE | TREATMENT PARTIALLY PROTECTS | WEIGHT-LOSS | NONALCOHOLIC STEATOHEPATITIS | DIET-INDUCED OBESITY | BUTYRATE-PRODUCING BACTERIA | INCREASED INTESTINAL PERMEABILITY | TOLL-LIKE RECEPTOR-4 | INNATE IMMUNITY | Choline - metabolism | Diabetes Mellitus, Type 2 - microbiology | Humans | Diabetes Mellitus, Type 1 - metabolism | Diabetes Mellitus, Type 2 - metabolism | Linoleic Acids, Conjugated - metabolism | Obesity - microbiology | Angiopoietin-like 4 Protein | Inflammation - metabolism | Diabetes Mellitus, Type 1 - etiology | Diabetes Mellitus, Type 1 - microbiology | Endotoxemia - microbiology | Cyclic AMP-Dependent Protein Kinases - metabolism | Angiopoietins - metabolism | Inflammation - microbiology | Carbohydrate Metabolism | Gastrointestinal Tract - microbiology | Rats | Bile Acids and Salts - metabolism | Toll-Like Receptor 4 - metabolism | Gastrointestinal Tract - metabolism | Obesity - metabolism | Animals | Energy Metabolism | Mice | Endotoxemia - metabolism | Metagenome | Physiological aspects | Homeostasis | Obesity | Diabetes | Microbiota (Symbiotic organisms) | Metabolism | Polyunsaturated fatty acids | Endotoxins | Lipids | Microflora | Toll-like receptors | Nutrients | Oxidation | Lipogenesis | Digestive tract | Bile acids | Techniques | Diabetes mellitus | Inflammation | Triglycerides | TLR4 protein | Fatty acids | Abdomen | Diets | Reviews | Diet | Barriers | Intestinal transit time
Journal Article
American Journal of Physiology - Gastrointestinal and Liver Physiology, ISSN 0193-1857, 12/2013, Volume 305, Issue 12, pp. G911 - G918
Journal Article
Journal of Gastroenterology and Hepatology, ISSN 0815-9319, 03/2009, Volume 24, Issue 3, pp. 443 - 452
Background and Aims:  We examined extrinsic and intrinsic (endogenous) mitochondrial apoptosis pathways in experimental non‐alcoholic steatohepatitis (NASH).... 
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 | FATTY LIVER-DISEASE | insulin-like growth factor-1 | NONALCOHOLIC STEATOHEPATITIS | PATHOGENESIS | HEPATIC INFLAMMATION | NECROSIS | MICE | TNF-ALPHA | GASTROENTEROLOGY & HEPATOLOGY | TRAIL-R killer | NF-KAPPA-B | 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
BBA - Molecular Basis of Disease, ISSN 0925-4439, 12/2017, Volume 1863, Issue 12, pp. 3170 - 3182
Journal Article