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1999
eJournal
Diabetes, obesity & metabolism, ISSN 1462-8902, 1999
Journal
Diabetes/metabolism reviews, ISSN 0742-4221, 1985
Journal
European Journal of Endocrinology, ISSN 0804-4643, 06/2017, Volume 176, Issue 6, pp. 685 - 693
Journal Article
The Journal of Clinical Endocrinology & Metabolism, ISSN 0021-972X, 03/2017, Volume 102, Issue 3, pp. 810 - 821
We found serum lipid profiles changed in women with PCOS. Obesity and compensatory hyperinsulinemia promoted the metabolism of arachidonic acid and other PUFAs, whereas androgen had an inhibitory effect. Abstract Context... 
POLYCYSTIC-OVARY-SYNDROME | IONIZATION-MASS-SPECTROMETRY | RISK-FACTORS | TESTOSTERONE | BIOLOGICAL SAMPLES | ENDOCRINOLOGY & METABOLISM | IMPAIRED GLUCOSE-TOLERANCE | NONALCOHOLIC STEATOHEPATITIS | FAT-CELL LIPOLYSIS | OLDER CHINESE | OBESE WOMEN | Arachidonic Acid - metabolism | Gas Chromatography-Mass Spectrometry | Linoleic Acid - metabolism | Humans | Dehydroepiandrosterone Sulfate - metabolism | Case-Control Studies | Young Adult | Testosterone - metabolism | Polycystic Ovary Syndrome - complications | Diet, High-Fat | Mass Spectrometry | Chromatography, Liquid | Adult | Female | Hyperandrogenism - metabolism | Fatty Acids - metabolism | Phosphatidylglycerols - metabolism | Disease Models, Animal | Hyperinsulinism - metabolism | Ceramides - metabolism | Hyperinsulinism - complications | Polycystic Ovary Syndrome - metabolism | Cholesterol, HDL - metabolism | Obesity - complications | Eicosapentaenoic Acid - metabolism | Rats | Sex Hormone-Binding Globulin - metabolism | Lipid Metabolism | Fatty Acids, Unsaturated - metabolism | Rats, Sprague-Dawley | Obesity - metabolism | Triglycerides - metabolism | Hyperandrogenism - complications | Insulin - metabolism | Animals | Cholesterol, LDL - metabolism | Phosphatidic Acids - metabolism | Androgens - metabolism | Blood Glucose - metabolism | Docosahexaenoic Acids - metabolism | Polycystic ovary syndrome | Obesity | Hyperinsulinemia | Lecithin | Polyunsaturated fatty acids | Lipids | Mass spectroscopy | Liquid chromatography | Phospholipids | Metabolism | Arachidonic acid | Insulin | Fatty acids | Patients | Chromatography | Biological activity | Subgroups | Gas chromatography | Androgens | Molecular modelling | Metabolites | Lipid metabolism | Mass spectrometry | Metabolic disorders
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 | 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
The Journal of clinical investigation, ISSN 0021-9738, 2013, Volume 123, Issue 4, pp. 1662 - 1676
Journal Article
Cell Metabolism, ISSN 1550-4131, 2005, Volume 2, Issue 6, pp. 373 - 384
Defective glucose-stimulated insulin secretion is the main cause of hyperglycemia in type 2 diabetes mellitus. Mutations in HNF-1α cause a monogenic form of... 
DIABETES-MELLITUS | HEPATOCYTE NUCLEAR FACTOR-1-ALPHA | MEMBRANE | ENDOCRINOLOGY & METABOLISM | FACTOR-I | MUTATIONS | SECRETION | TRANSCRIPTION FACTOR | CELL | MOLECULAR-MECHANISMS | ALPHA-GENE | CELL BIOLOGY | Immunohistochemistry | Immunoprecipitation | Membrane Glycoproteins - metabolism | Oligonucleotide Array Sequence Analysis | Calcium - metabolism | Humans | Insulinoma | Molecular Sequence Data | Immunoblotting | Diabetes Mellitus, Type 2 - metabolism | Exocytosis | RNA, Messenger - metabolism | Microscopy, Immunoelectron | Tissue Distribution | Insulin-Secreting Cells - metabolism | Time Factors | Base Sequence | Islets of Langerhans - cytology | Cloning, Molecular | Transcription, Genetic | Insulin Secretion | Genes, Reporter | Disease Models, Animal | Cell Line | Nucleic Acid Hybridization | Growth Hormone - metabolism | Hepatocyte Nuclear Factor 1 - metabolism | Glutathione Transferase - metabolism | Rats | Mice, Transgenic | Photons | Pancreas - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Two-Hybrid System Techniques | Blotting, Northern | Insulin - metabolism | Animals | Glucose - chemistry | Glucose - metabolism | Protein Binding | Mice | Models, Genetic | DNA, Complementary - metabolism | SNARE Proteins - metabolism | Microscopy, Fluorescence | RNA, Small Interfering - metabolism | Type 2 diabetes | Medical colleges | Pancreatic beta cells | Hyperglycemia | Molecular genetics | Insulin | Protein binding | Diabetes therapy
Journal Article
Cell metabolism, ISSN 1550-4131, 2012, Volume 16, Issue 5, pp. 625 - 633
Journal Article
Nature communications, ISSN 2041-1723, 2018, Volume 9, Issue 1, pp. 546 - 9
Journal Article
Diabetes, ISSN 0012-1797, 11/2011, Volume 60, Issue 11, pp. 2872 - 2882
OBJECTIVE-To evaluate whether healthy or diabetic adult mice can tolerate an extreme loss of pancreatic a-cells and how this sudden massive depletion affects... 
INSULIN | HYPERGLUCAGONEMIA | ENDOCRINE PANCREAS | GLUCOSE-HOMEOSTASIS | ENDOCRINOLOGY & METABOLISM | RECEPTOR GENE | SECRETION | DIFFERENTIATION | HYPERPLASIA | ISLET CELLS | EXPRESSION | Insulin-Secreting Cells - secretion | Apoptosis - drug effects | Cell Count | Glucagon - genetics | Male | Diphtheria Toxin - toxicity | Insulin - blood | Glucagon - blood | Diabetes Mellitus, Experimental - blood | Hypoglycemia - prevention & control | Intercellular Signaling Peptides and Proteins - metabolism | Glucagon-Secreting Cells - drug effects | Insulin-Secreting Cells - metabolism | Hyperglycemia - chemically induced | Glucagon-Secreting Cells - metabolism | Diabetes Mellitus, Experimental - chemically induced | Diabetes Mellitus, Experimental - metabolism | Glucagon-Secreting Cells - secretion | Hyperglycemia - prevention & control | Promoter Regions, Genetic | Signal Transduction | Glucagon-Secreting Cells - pathology | Intercellular Signaling Peptides and Proteins - genetics | Pancreas - drug effects | Pancreas - pathology | Receptors, Glucagon - metabolism | Mice, Transgenic | Pancreas - metabolism | Heparin-binding EGF-like Growth Factor | Insulin - metabolism | Animals | Insulin-Secreting Cells - drug effects | Tamoxifen - pharmacology | Diabetes Mellitus, Experimental - pathology | Glucagon - metabolism | Mice | Streptozocin - toxicity | Insulin-Secreting Cells - pathology | Selective Estrogen Receptor Modulators - pharmacology | Islet Studies
Journal Article
The Journal of Physiology, ISSN 0022-3751, 2004, Volume 556, Issue 3, pp. 983 - 1000
Muscular adaptation to physical exercise has previously been described as a repair process following tissue damage. Recently, evidence has been published to... 
INDUCED INJURY | PHYSIOLOGY | IMMUNOREACTIVITY | ECCENTRIC EXERCISE | REGENERATION | LEUKEMIA INHIBITORY FACTOR | DENERVATED HUMAN MUSCLE | SATELLITE CELLS | STRENGTH | FACTOR-I | EXPRESSION | NEUROSCIENCES | Immunohistochemistry | Granulocytes - cytology | Cytokines - analysis | Humans | Middle Aged | DNA-Binding Proteins - analysis | Ki-67 Antigen - metabolism | Male | Muscle, Skeletal - metabolism | Proteins - analysis | Pain - metabolism | fas Receptor - metabolism | Fascia - chemistry | Oxygen Consumption - physiology | fas Receptor - analysis | Antigens, CD - metabolism | Antigens, CD - analysis | Running - physiology | C-Reactive Protein - metabolism | Aryl Hydrocarbon Receptor Nuclear Translocator | CD11b Antigen - analysis | Receptors, Cytokine - metabolism | Testosterone - blood | C-Reactive Protein - analysis | Hormones - blood | Leukocytes - chemistry | Interleukin-6 - metabolism | Lymphocytes - metabolism | CD56 Antigen - analysis | Lymphocytes - cytology | Insulin-Like Growth Factor I - analysis | Muscle, Skeletal - physiology | CD3 Complex - metabolism | Leukemia Inhibitory Factor Receptor alpha Subunit | Regression Analysis | Pain - physiopathology | Receptors, Cytokine - analysis | Adolescent | Antigens, Differentiation, Myelomonocytic - analysis | Creatine Kinase - metabolism | Transcription Factors - analysis | Leukocytes - metabolism | Insulin-Like Growth Factor I - metabolism | Receptors, OSM-LIF | Interleukin-6 - analysis | Monocytes - cytology | Receptors, Cell Surface - analysis | Monocytes - metabolism | Receptors, Aryl Hydrocarbon - analysis | DNA-Binding Proteins - metabolism | Testosterone - metabolism | Flow Cytometry | Interleukin-6 - blood | Exercise Test - methods | Muscle, Skeletal - chemistry | Fascia - metabolism | Heart Rate - physiology | Receptors, Aryl Hydrocarbon - metabolism | Adult | Female | Leukocyte Count | Leukemia Inhibitory Factor | Isometric Contraction - physiology | Cytokines - blood | Leukocytes - cytology | CD56 Antigen - metabolism | Creatine Kinase - blood | Cytokines - metabolism | Receptors, Cell Surface - metabolism | Transcription Factors - metabolism | CD3 Complex - analysis | Ki-67 Antigen - analysis | Proteins - metabolism | Hormones - metabolism | Antigens, Differentiation, Myelomonocytic - metabolism | CD11b Antigen - metabolism | Growth Substances - metabolism | Pain - diagnosis | Research Papers
Journal Article
Nature communications, ISSN 2041-1723, 2013, Volume 4, Issue 1, p. 1829
Journal Article