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Molecular Nutrition & Food Research, ISSN 1613-4125, 08/2015, Volume 59, Issue 8, pp. 1443 - 1457
ScopeResveratrol (RSV), a natural polyphenol, has been reported to attenuate nonalcoholic fatty liver disease (NAFLD); however, its underlying mechanism is... 
NAFLD | Treatment | Hepatocyte | SIRT1 | Resveratrol | ACTIVATION | LIPID-METABOLISM | PROTEIN-KINASE | FOOD SCIENCE & TECHNOLOGY | NONALCOHOLIC FATTY LIVER | DIET | INFLAMMATION | DISEASE | AMPK | HEALTH | Sirtuin 1 - metabolism | Non-alcoholic Fatty Liver Disease - pathology | Liver - pathology | Stilbenes - therapeutic use | Antioxidants - metabolism | Humans | Stilbenes - metabolism | Mice, 129 Strain | Sirtuin 1 - genetics | Autophagy - drug effects | Fatty Acids, Nonesterified - metabolism | Liver - drug effects | RNA Interference | Enzyme Induction - drug effects | Sirtuin 1 - chemistry | Cyclic AMP - metabolism | Fatty Acids, Nonesterified - adverse effects | Microscopy, Electron, Transmission | Second Messenger Systems - drug effects | Liver - ultrastructure | Liver - metabolism | Enzyme Inhibitors - pharmacology | Non-alcoholic Fatty Liver Disease - metabolism | Adenylyl Cyclases - metabolism | Sirtuin 1 - antagonists & inhibitors | Hep G2 Cells | Cyclic AMP - antagonists & inhibitors | Antioxidants - therapeutic use | Animals | Adenylyl Cyclases - chemistry | Lipid Metabolism - drug effects | Fatty Acids, Nonesterified - antagonists & inhibitors | Cyclic AMP - agonists | Non-alcoholic Fatty Liver Disease - diet therapy | Adenylyl Cyclases - genetics | Dietary Supplements | Triglycerides | Liver diseases | Fatty acids | Liver | Index Medicus
Journal Article
Biochemical Pharmacology, ISSN 0006-2952, 08/2017, Volume 138, pp. 140 - 149
Pancreatic β-cell lipotoxicity is a central feature of the pathogenesis of type 2 diabetes. To study the mechanism by which fatty acids cause β-cell death and... 
Beta-cell | Islet | Diabetes | Lipotoxicity | HUMAN PANCREATIC-ISLETS | ELASTIC NET | ACTIVATION | CANCER CELLS | RAT | ENDOPLASMIC-RETICULUM STRESS | PATHWAY | GLUCOSE | PHARMACOLOGY & PHARMACY | MAP4K4 | Islets of Langerhans - drug effects | Insulin-Secreting Cells - secretion | Rats, Wistar | Apoptosis - drug effects | Humans | Male | Intracellular Signaling Peptides and Proteins - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Islets of Langerhans - secretion | Insulin-Secreting Cells - metabolism | RNA Interference | Islets of Langerhans - metabolism | Islets of Langerhans - cytology | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Female | Insulin-Secreting Cells - cytology | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Fatty Acids, Nonesterified - adverse effects | Recombinant Proteins - metabolism | Cell Line | Tissue Culture Techniques | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | Cells, Cultured | Computational Biology | Enzyme Inhibitors - pharmacology | Protein-Serine-Threonine Kinases - genetics | Recombinant Proteins - chemistry | Hypoglycemic Agents - pharmacology | Phosphatidylinositol 3-Kinases - genetics | Animals | Class I Phosphatidylinositol 3-Kinases | High-Throughput Screening Assays | Insulin-Secreting Cells - drug effects | Small Molecule Libraries | Fatty Acids, Nonesterified - antagonists & inhibitors | Protein Kinase Inhibitors - pharmacology | Index Medicus
Journal Article
Diabetes, Obesity and Metabolism, ISSN 1462-8902, 09/2017, Volume 19, Issue 9, pp. 1306 - 1311
In view of the occurrence of diabetic ketoacidosis associated with the use of sodium‐glucose transport protein‐2 inhibitors in patients with type 1 diabetes (... 
liraglutide | type 1 diabetes | insulin | ketogenesis | EFFICACY | GHRELIN | ADJUNCT | RANDOMIZED-TRIAL | ADDITIONAL TREATMENT | MELLITUS | INSULIN-TREATMENT | PEPTIDE-1 | ENDOCRINOLOGY & METABOLISM | HYPOGLYCEMIA | HORMONE RESPONSES | Lipolysis - drug effects | Humans | Middle Aged | Diabetes Mellitus, Type 1 - metabolism | Male | Glucagon - blood | Glucagon - antagonists & inhibitors | Glucagon-Like Peptide-1 Receptor - metabolism | Hypoglycemic Agents - administration & dosage | Injections, Subcutaneous | Adult | Fatty Acids, Nonesterified - blood | Female | Insulin Infusion Systems | Ketone Bodies - antagonists & inhibitors | Drug Therapy, Combination | Drug Resistance | Hypoglycemic Agents - therapeutic use | Ketone Bodies - biosynthesis | Double-Blind Method | Insulin - administration & dosage | Diabetes Mellitus, Type 1 - drug therapy | Ghrelin - antagonists & inhibitors | Ghrelin - blood | Ketone Bodies - blood | Diabetes Mellitus, Type 1 - blood | Liraglutide - therapeutic use | Fatty Acids, Nonesterified - antagonists & inhibitors | Liraglutide - administration & dosage | Glucagon-Like Peptide-1 Receptor - agonists | Insulin - therapeutic use | Medicine, Experimental | Medical research | Glucagon | Type 1 diabetes | Fatty acids | Ketogenesis | Diabetes mellitus | Glucose | Glucose transport | Insulin | Lipolysis | Sodium | Ghrelin | Ketoacidosis | Diabetes | Protein transport | Index Medicus
Journal Article
Circulation, ISSN 0009-7322, 11/2006, Volume 114, Issue 20, pp. 2130 - 2137
Journal Article
Molecular Nutrition & Food Research, ISSN 1613-4125, 10/2014, Volume 58, Issue 10, pp. 2053 - 2065
Scope: To investigate whether docosahexaenoic acid (DHA) could inhibit linoleic acid (LA) induced monocyte chemoattractant protein (MCP)-1 expression in human... 
Monocyte chemoattractant protein‐1 | Neovascularization | Docosahexaenoic acid | Peroxisome proliferator‐activated receptors | Linoleic acid | Monocyte chemoattractant protein-1 | Peroxisome proliferator-activated receptors | AORTIC ENDOTHELIAL-CELLS | PROLIFERATOR-ACTIVATED RECEPTORS | FOOD SCIENCE & TECHNOLOGY | KINASE | MACULAR DEGENERATION | ALPHA | DIETARY FATTY-ACIDS | CHOROIDAL NEOVASCULARIZATION | ADHESION | GENE | INFLAMMATION | Retinal Pigment Epithelium - metabolism | Arachidonic Acid - adverse effects | Macular Degeneration - immunology | Retinal Pigment Epithelium - secretion | Humans | Choroidal Neovascularization - etiology | NF-kappa B - metabolism | PPAR gamma - metabolism | Promoter Regions, Genetic - drug effects | Arachidonic Acid - antagonists & inhibitors | Linoleic Acid - adverse effects | Linoleic Acid - antagonists & inhibitors | Osmolar Concentration | Chemokine CCL2 - metabolism | Choroid - drug effects | Fatty Acids, Nonesterified - adverse effects | PPAR gamma - genetics | Retinal Pigment Epithelium - drug effects | Docosahexaenoic Acids - therapeutic use | Macular Degeneration - etiology | Cell Line | Macular Degeneration - prevention & control | Choroid - metabolism | Choroidal Neovascularization - immunology | Eicosapentaenoic Acid - metabolism | Chemokine CCL2 - genetics | Choroidal Neovascularization - prevention & control | Up-Regulation - drug effects | Macular Degeneration - metabolism | Choroidal Neovascularization - metabolism | PPAR gamma - antagonists & inhibitors | NF-kappa B - genetics | Signal Transduction - drug effects | Retinal Pigment Epithelium - immunology | Anilides - pharmacology | Fatty Acids, Nonesterified - antagonists & inhibitors | Chemokine CCL2 - agonists | Choroid - immunology | Eicosapentaenoic Acid - therapeutic use | Chemokine CCL2 - antagonists & inhibitors | Culture Media, Conditioned - metabolism | Docosahexaenoic Acids - metabolism | Index Medicus
Journal Article
Cellular Physiology and Biochemistry, ISSN 1015-8987, 07/2017, Volume 42, Issue 4, pp. 1635 - 1644
Background: This study aimed to investigate whether exogenous hydrogen sulfide (H2S) can protect the RAW264.7 macrophages against the inflammation induced by... 
Inflammation | Macrophages | Free Fatty Acids | Exogenous Hydrogen Sulfide | PATHWAYS | ACTIVATION | PHYSIOLOGY | INJURY | MECHANISMS | NLRP3 INFLAMMASOME | CELL BIOLOGY | OBESITY | INSULIN-RESISTANCE | RECEPTORS | EXPRESSION | ADIPOSE-TISSUE | Interleukin-18 - immunology | Inflammasomes - metabolism | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | NF-kappa B - immunology | Sulfides - chemistry | Caspase 3 - immunology | Anti-Inflammatory Agents, Non-Steroidal - chemistry | Fatty Acids, Nonesterified - pharmacology | Interleukin-1beta - genetics | Anti-Inflammatory Agents, Non-Steroidal - pharmacology | NLR Family, Pyrin Domain-Containing 3 Protein - genetics | Caspase 3 - genetics | Toll-Like Receptor 4 - antagonists & inhibitors | Macrophages - immunology | Sulfides - pharmacology | Cell Line | Cell Survival - drug effects | Hydrogen Sulfide - pharmacology | NF-kappa B - antagonists & inhibitors | Signal Transduction | Hydrogen Sulfide - chemistry | Gene Expression Regulation | Interleukin-1beta - immunology | Toll-Like Receptor 4 - genetics | Toll-Like Receptor 4 - immunology | Macrophages - cytology | Reactive Oxygen Species - antagonists & inhibitors | Animals | NLR Family, Pyrin Domain-Containing 3 Protein - immunology | NF-kappa B - genetics | Inflammasomes - immunology | Fatty Acids, Nonesterified - antagonists & inhibitors | Macrophages - drug effects | Mice | Interleukin-18 - genetics | Proteins | Cell culture | Cell growth | Sodium | Hydrogen | Hypoxia | Glucose | Metabolic syndrome | Fatty acids | Variance analysis | Apoptosis | Index Medicus
Journal Article
Journal Article
The Journal of Physiology, ISSN 0022-3751, 06/2013, Volume 591, Issue 11, pp. 2897 - 2909
Journal Article
Biochemistry and Cell Biology, ISSN 0829-8211, 2015, Volume 93, Issue 6, pp. 566 - 573
Nonalcoholic fatty liver disease (NAFLD) describes a spectrum of lesions ranging from simple steatosis to non-alcoholic steatohepatitis (NASH). The excess... 
steatohepatitis | stéatohépatite | lactoferrin | apoptosis | Akt | apoptose | lactoferrine | cytotoxicity | cytotoxicité | Cytotoxicity | Lactoferrin | Steatohepatitis | Apoptosis | VISCERAL FAT | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | LIVER-DISEASE | CELL BIOLOGY | CYTOCHROME-C | LIPID-ACCUMULATION | IN-VITRO | INSULIN-RESISTANCE | HEPG2 CELLS | BOVINE LACTOFERRIN | Non-alcoholic Fatty Liver Disease - pathology | Liver - pathology | Apoptosis - drug effects | Humans | JNK Mitogen-Activated Protein Kinases - metabolism | Peptide Fragments - pharmacology | Quinoxalines - pharmacology | Fatty Acids, Nonesterified - metabolism | Lipotropic Agents - metabolism | Lactoferrin - pharmacology | Liver - drug effects | Protein Processing, Post-Translational - drug effects | Cattle | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Fatty Acids, Nonesterified - adverse effects | Lactoferrin - metabolism | Peptide Fragments - metabolism | JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors | Lipotropic Agents - chemistry | Liver - metabolism | Non-alcoholic Fatty Liver Disease - metabolism | Anthracenes - pharmacology | Hep G2 Cells | Lactoferrin - chemistry | Peptide Fragments - chemistry | Animals | MAP Kinase Signaling System - drug effects | Proto-Oncogene Proteins c-akt - agonists | Lipid Metabolism - drug effects | Non-alcoholic Fatty Liver Disease - prevention & control | Fatty Acids, Nonesterified - antagonists & inhibitors | Benzimidazoles - pharmacology | Lipotropic Agents - pharmacology | Lactoferrin - antagonists & inhibitors | Protein Kinase Inhibitors - pharmacology | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Development and progression | Cellular signal transduction | Genetic aspects | Liver diseases | Health aspects | Lactoferrins | Signal transduction | Carcinogens | Phosphorylation | Glycoproteins | Fatty acids | Index Medicus
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Journal Article
Journal Article