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1. Full Text Propylselen inhibits cancer cell growth by targeting glutamate dehydrogenase at the NADP+ binding site
by Hou, Wei and Lu, Shiying and Zhao, Han and Yu, Yan and Yu, Biao and Xu, Haodong and Su, Lin and Lin, Chenshui and Ruan, Benfang Helen
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 01/2019, Volume 509, Issue 1, pp. 262 - 267
High levels of glutamate dehydrogenase (GDH) activity are associated with hypoglycemia, cancer, and Parkinson's disease. Propylselen was synthesized to... 
Glutamate dehydrogenase | Propylselen | Biomolecular interaction assay | Inhibitors | Enzyme kinetics | EGCG | ALLOSTERIC REGULATION | ENZYME | BIOPHYSICS | GLUTAMINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | HYPERINSULINISM
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2. Full Text Variations in adrenal gland medulla and dopamine effects induced by the lack of Irs2
by Catalano-Iniesta, Leonardo and Iglesias-Osma, María Carmen and Sánchez-Robledo, Virginia and Carretero-Hernández, Marta and Blanco, Enrique J and Carretero, José and García-Barrado, María José
Journal of Physiology and Biochemistry, ISSN 1138-7548, 11/2018, Volume 74, Issue 4, pp. 667 - 677
The adrenomedullary chromaffin cells' hormonal pathway has been related to the pathophysiology of diabetes mellitus. In mice, the deletion of insulin receptor... 
Glycerol release | Dopamine | Beta-cells | Adrenal chromaffin cells | Tyrosine hydroxylase | Adipocytes | Proliferation | Apoptosis | Insulin secretion | PHYSIOLOGY | BIOCHEMISTRY & MOLECULAR BIOLOGY | NEUROENDOCRINE | CATECHOLAMINE SECRETION | DIABETIC-NEUROPATHY | DEFICIENCY | HYPOGLYCEMIA | NEURONS | PROTEINS | Prediabetic State - metabolism | Adrenal Medulla - metabolism | Tyrosine 3-Monooxygenase - metabolism | Chromaffin Cells - enzymology | Chromaffin Cells - pathology | Male | Insulin Receptor Substrate Proteins - metabolism | Islets of Langerhans - metabolism | Female | Prediabetic State - pathology | Insulin Receptor Substrate Proteins - genetics | Hyperinsulinism - blood | Insulin Secretion | Dopamine - metabolism | Hyperinsulinism - metabolism | Prediabetic State - blood | Adrenal Medulla - pathology | Islets of Langerhans - pathology | Tissue Culture Techniques | Mice, Inbred C57BL | Cells, Cultured | Organ Size | Adrenal Medulla - enzymology | Sex Characteristics | Lipolysis | Mice, Knockout | Hyperinsulinism - pathology | Chromaffin Cells - metabolism | Adipocytes, White - pathology | Animals | In Vitro Techniques | Adipocytes, White - metabolism | Immunohistochemistry | Tyrosine | Analysis | Phenols | Insulin resistance | Diabetes | Cells
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3. Full Text Quantitative Proteomic Analysis of Hepatic Tissue of T2DM Rhesus Macaque
by Du, Tingfu and Lu, Shuaiyao and Jiang, Qinfang and Li, Yun and Ma, Kaili
Journal of Diabetes Research, ISSN 2314-6745, 2017, Volume 2017, pp. 3601708 - 10
Type 2 diabetes mellitus (T2DM) is a metabolic disorder that severely affects human health, but the pathogenesis of the disease remains unknown. The... 
C-REACTIVE PROTEIN | MEDICINE, RESEARCH & EXPERIMENTAL | HIGH-FAT | METABOLISM | INSULIN-RESISTANCE | ACID-BINDING PROTEIN | ENDOCRINOLOGY & METABOLISM | RISK | GLUCOKINASE | TYPE-2 DIABETES-MELLITUS | GLUCOSE-TOLERANCE | LIVER FAT | Liver - pathology | Liver - enzymology | Kidney - pathology | Gene Expression Profiling | Macaca mulatta | Chromatography, High Pressure Liquid | Diabetes Mellitus, Type 2 - metabolism | Tandem Mass Spectrometry | Spectrometry, Mass, Electrospray Ionization | Hyperinsulinism - etiology | Peptide Mapping | Female | Obesity - etiology | Proteomics - methods | Real-Time Polymerase Chain Reaction | Diabetes Mellitus, Type 2 - complications | Hyperlipidemias - complications | Hyperinsulinism - metabolism | Hyperinsulinism - complications | Hyperlipidemias - metabolism | Obesity - complications | Liver - metabolism | Computational Biology | Insulin Resistance | Pancreas - pathology | Reverse Transcriptase Polymerase Chain Reaction | Diet, Western - adverse effects | Obesity - metabolism | Obesity - pathology | Gene Expression Regulation - drug effects | Hyperinsulinism - pathology | Animals | Hyperlipidemias - etiology | Hyperlipidemias - pathology | Diabetes Mellitus, Type 2 - pathology
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4. Full Text Bile acid TUDCA improves insulin clearance by increasing the expression of insulin-degrading enzyme in the liver of obese mice
by Vettorazzi, Jean Franciesco and Kurauti, Mirian Ayumi and Soares, Gabriela Moreira and Borck, Patricia Cristine and Ferreira, Sandra Mara and Branco, Renato Chaves Souto and Michelone, Luciana De Souza Lima and Boschero, Antonio Carlos and Junior, Jose Maria Costa and Carneiro, Everardo Magalhães
Scientific Reports, ISSN 2045-2322, 12/2017, Volume 7, Issue 1, pp. 14876 - 9
Disruption of insulin secretion and clearance both contribute to obesity-induced hyperinsulinemia, though reduced insulin clearance seems to be the main... 
METABOLIC SYNDROME | ALZHEIMERS-DISEASE | GLUCOSE | MULTIDISCIPLINARY SCIENCES | RESISTANCE | FAT | BARIATRIC SURGERY | HYPERINSULINEMIA | DEGRADATION | INHIBITORS | SECRETION | Insulysin - metabolism | Liver - enzymology | Humans | Liver - metabolism | Hyperinsulinism - drug therapy | Hep G2 Cells | Taurochenodeoxycholic Acid - pharmacology | Insulysin - drug effects | Animals | Diet, High-Fat | Mice, Obese | Mice | Insulin - pharmacokinetics | Taurine | Hyperinsulinemia | Obesity | Enzymes | Secretion | Liver | Insulysin | AKT protein | Insulin | Bile | High fat diet | 1-Phosphatidylinositol 3-kinase
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5. Full Text Relationship between circulating levels of pancreatic proteolytic enzymes and pancreatic hormones
by Bharmal, Sakina H and Pendharkar, Sayali A and Singh, Ruma G and Goodarzi, Mark O and Pandol, Stephen J and Petrov, Maxim S
Pancreatology, ISSN 1424-3903, 11/2017, Volume 17, Issue 6, pp. 876 - 883
While the close morphological relationship between the exocrine and endocrine pancreas is well established, their functional interaction remains poorly... 
Insulo-acinar axis | Chymotrypsin | Trypsin | Pancreatic hormones | Insulin | ISLET BLOOD-FLOW | CATIONIC TRYPSIN | ENDOCRINE | RATS | RECEPTOR DOWN-REGULATION | EXOCRINE PANCREAS | ABDOMINAL OBESITY | GLUCOSE-METABOLISM | INSULIN-RESISTANCE | SCANNING-ELECTRON-MICROSCOPY | GASTROENTEROLOGY & HEPATOLOGY | Diabetes Mellitus - blood | Cross-Sectional Studies | Humans | Middle Aged | Diabetes Mellitus - metabolism | Male | Insulin - blood | Pancreatitis - enzymology | Chymotrypsin - blood | Pancreatitis - blood | Trypsin - blood | Adult | Female | Aged | Hyperinsulinism - blood | Pancreas - enzymology | Enzymes | Pancreatic hormone | Polypeptides | Metabolic diseases | Dosage and administration | Research | Health aspects | Hyperinsulinemia | Statistical analysis | Glucagon | Proteolytic enzymes | Diabetes mellitus | Pancreatitis | Hormones | Glucose | Studies | Body mass index | Proteolysis | Rodents | Mathematical models | Somatostatin | Smoking
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6. Full Text Intramuscular triglyceride content precedes impaired glucose metabolism without evidence for mitochondrial dysfunction during early development of a diabetic phenotype
by Oxendine, Michael J and Schaeffer, Paul J and Callahan, Zachary J
Applied Physiology, Nutrition, and Metabolism, ISSN 1715-5312, 2017, Volume 42, Issue 9, pp. 963 - 972
The incidence of type 2 diabetes is highly correlated with obesity; however, there is a lack of research elucidating the temporal progression. Transgenic FVB/N... 
nuclear receptors | diabète | obésité | lipotoxicity | lipotoxicité | récepteurs nucléaires | diabetes | obesity | Obesity | Diabetes | Lipotoxicity | Nuclear receptors | CAPACITY | SPORT SCIENCES | PHYSIOLOGY | LIPID-CONTENT | SENSITIVITY | BROWN ADIPOSE-TISSUE | HUMAN SKELETAL-MUSCLE | NUTRITION & DIETETICS | MUSCLE INSULIN-RESISTANCE | FATTY-ACID OXIDATION | TRANSGENIC MICE | Mitochondrial Dynamics | Prediabetic State - metabolism | Weaning | Mitochondria, Muscle - metabolism | Diet, High-Fat - adverse effects | Male | Muscle, Skeletal - metabolism | Diabetes Mellitus, Type 2 - metabolism | Obesity - blood | Adiposity | Hyperinsulinism - etiology | Time Factors | Diabetes Mellitus, Type 2 - etiology | Obesity - etiology | Prediabetic State - etiology | Weight Gain | Hyperinsulinism - blood | Hyperinsulinism - physiopathology | Hyperinsulinism - metabolism | Muscle, Skeletal - enzymology | Prediabetic State - blood | Reproducibility of Results | Mitochondria, Muscle - enzymology | Insulin Resistance | Mice, Transgenic | Obesity - physiopathology | Random Allocation | Disease Progression | Obesity - metabolism | Triglycerides - metabolism | Diabetes Mellitus, Type 2 - blood | Animals | Prediabetic State - physiopathology | Type 2 diabetes | Physiological aspects | Development and progression | Genetic aspects | Triglycerides | Research
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7. Full Text Precision medicine in rare disease: Mechanisms of disparate effects of N-carbamyl-l-glutamate on mutant CPS1 enzymes
by Shi, Dashuang and Zhao, Gengxiang and Ah Mew, Nicholas and Tuchman, Mendel
Molecular Genetics and Metabolism, ISSN 1096-7192, 03/2017, Volume 120, Issue 3, pp. 198 - 206
This study documents the disparate therapeutic effect of -carbamyl- -glutamate (NCG) in the activation of two different disease-causing mutants of carbamyl... 
Urea cycle disorder, mutations | Carbamyl phosphate synthetase 1 deficiency | Hyperammonemia | N-acetyl-l-glutamate | N-acetyl-L-glutamate | PROPIONIC ACIDEMIA | MEDICINE, RESEARCH & EXPERIMENTAL | ACETYLGLUTAMATE SYNTHASE DEFICIENCY | HYPERINSULINISM/HYPERAMMONEMIA SYNDROME | PHOSPHATE SYNTHETASE-I | RAT-LIVER MITOCHONDRIA | RECOMBINANT CPS1 | CARGLUMIC ACID | MAMMALIAN LIVER | ENDOCRINOLOGY & METABOLISM | GENETICS & HEREDITY | NEONATAL HYPERAMMONEMIA | METHYLMALONIC ACIDURIA | Protein Structure, Tertiary | Adenosine Triphosphate - administration & dosage | Humans | Rare Diseases - drug therapy | Male | Carbamoyl-Phosphate Synthase (Ammonia) - chemistry | Rare Diseases - enzymology | Adenosine Triphosphate - pharmacology | Animals | Carbamoyl-Phosphate Synthase I Deficiency Disease - drug therapy | Carbamoyl-Phosphate Synthase I Deficiency Disease - enzymology | Protein Stability - drug effects | Glutamates - pharmacology | Glutamates - administration & dosage | Female | Mice | Mutation | Drug Therapy, Combination | Carbamoyl-Phosphate Synthase (Ammonia) - genetics | Precision Medicine | Glutamate | Enzymes | Analysis | Phosphates | Urea | Amino acids | Ligases | Urea cycle disorder | mutations
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8. Full Text Salvianolic Acid B Ameliorates Hyperglycemia and Dyslipidemia in db/db Mice through the AMPK Pathway
by Huang, Ming-Qing and Zhou, Cai-Jie and Zhang, Yi-Ping and Zhang, Xiao-Qin and Xu, Wen and Lin, Jing and Wang, Pei-Jian
Cellular Physiology and Biochemistry, ISSN 1015-8987, 12/2016, Volume 40, Issue 5, pp. 933 - 943
Background/Aims: Salvianolic acid B (Sal B), a major polyphenolic compound of Salvia miltiorrhiza Bunge, has been shown to possess potential antidiabetic... 
Original Paper | AMPK | GLUT4 | PPARa | Type 2 Diabetes | Salvianolic acid B | APOPTOSIS | PHYSIOLOGY | ACTIVATED PROTEIN-KINASE | PPAR alpha | BIOLOGICAL-ACTIVITIES | MILTIORRHIZA | CELL BIOLOGY | PRODUCT | PHARMACOLOGY | ANIMAL-MODELS | CHEMISTRY | STREPTOZOTOCIN | EXPRESSION | Dyslipidemias - genetics | AMP-Activated Protein Kinases - metabolism | Dyslipidemias - complications | Glucose Transporter Type 4 - metabolism | Glycogen Synthase - metabolism | Gluconeogenesis - drug effects | Body Weight - drug effects | Hyperglycemia - complications | Benzofurans - pharmacology | Male | Hyperinsulinism - drug therapy | RNA, Messenger - metabolism | Glycolysis - drug effects | Hyperglycemia - drug therapy | Glucose Intolerance - blood | Hyperglycemia - genetics | Benzofurans - chemistry | Glucose Intolerance - drug therapy | Dyslipidemias - blood | Glycogen - metabolism | Liver - drug effects | Lipids - blood | Muscle, Skeletal - drug effects | Phosphorylation - drug effects | Hyperinsulinism - blood | Dyslipidemias - drug therapy | Glucose Intolerance - genetics | Muscle, Skeletal - enzymology | Benzofurans - therapeutic use | Hyperinsulinism - complications | Liver - metabolism | Mice, Inbred C57BL | RNA, Messenger - genetics | Pancreas - drug effects | Pancreas - pathology | Glucose Intolerance - complications | Gene Expression Regulation - drug effects | Animals | Hyperglycemia - blood | Signal Transduction - drug effects | Glucose - metabolism | PPAR alpha - metabolism | PPARα
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9. Full Text Differential regulation of pancreatic digestive enzymes during chronic high-fat diet-induced obesity in C57BL/6J mice
by Birk, R.Z and Rubio-Aliaga, I and Boekschoten, M.V and Danino, H and Müller, M.R and Daniel, H
The British journal of nutrition, ISSN 0007-1145, 2014, Volume 112, Issue 2, pp. 154 - 161
Exocrine pancreatic digestive enzymes are essential for the digestion of dietary components and are regulated by them. Chronic excess dietary high fat (HF)... 
2 related proteins | insulin-resistance | expression | colipase | cholesterol absorption | lipase messenger-rna | cholecystokinin | adaptation | exocrine pancreas | rats | Obesity | Exocrine pancreas | Digestive enzymes | CHOLECYSTOKININ | RATS | LIPASE MESSENGER-RNA | 2 RELATED PROTEINS | CHOLESTEROL ABSORPTION | NUTRITION & DIETETICS | INSULIN-RESISTANCE | ADAPTATION | COLIPASE | EXPRESSION | Diet, High-Fat - adverse effects | Male | RNA, Messenger - metabolism | Phospholipases A2, Secretory - genetics | Leptin - blood | Hyperinsulinism - etiology | Obesity - etiology | Colipases - genetics | RNA Processing, Post-Transcriptional | Mice, Inbred C57BL | Insulin Resistance | Obesity - physiopathology | Lipase - metabolism | Random Allocation | Pancreas, Exocrine - enzymology | Obesity - metabolism | Gene Expression Regulation, Enzymologic | Animals | Hyperglycemia - etiology | Mice | Obesity - enzymology | Pancreas, Exocrine - metabolism | Pancreas, Exocrine - physiopathology | Phospholipases A2, Secretory - metabolism | Protein Processing, Post-Translational | Colipases - metabolism | Lipase - genetics | Enzymes | Nutrition research | Oils & fats | Rodents
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10. Full Text Relationship between pancreatic hormones and glucose metabolism: A cross-sectional study in patients after acute pancreatitis
by Pendharkar, SA and Asrani, VM and Xiao, AY and Yoon, HD and Murphy, R and Windsor, JA and Petrov, MS
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, ISSN 0193-1857, 07/2016, Volume 311, Issue 1, pp. G50 - G58
Abnormal glucose metabolism is present in almost 40% of patients after acute pancreatitis, but its pathophysiology has been poorly investigated. Pancreatic... 
PHYSIOLOGY | RISK-FACTORS | insulin | POLYPEPTIDE CONCENTRATIONS | ENDOCRINE | CLASSIFICATION | PREVALENCE | EXOCRINE | DIABETES-MELLITUS | acute pancreatitis | amylin | pancreatic polypeptide | SECRETION | ALCOHOLIC PANCREATITIS | GASTROENTEROLOGY & HEPATOLOGY | glucose metabolism | Multivariate Analysis | Glycated Hemoglobin A - metabolism | Humans | Middle Aged | Male | Pancreatitis - complications | Insulin - blood | Glucagon - blood | Pancreatic Hormones - blood | Hyperinsulinism - etiology | Fasting - blood | Adult | Female | Hyperinsulinism - blood | Acute Disease | Cross-Sectional Studies | Insulin Resistance | Linear Models | Biomarkers - blood | Chi-Square Distribution | Islet Amyloid Polypeptide - blood | Pancreatitis - diagnosis | Pancreatitis - enzymology | Pancreatic Polypeptide - blood | Somatostatin - blood | Pancreatitis - blood | Aged | Blood Glucose - metabolism
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11. Full Text Enhanced islet cell nucleomegaly defines diffuse congenital hyperinsulinism in infancy but not other forms of the disease
by Han, Bing and Newbould, Melanie and Batra, Gauri and Cheesman, Edmund and Craigie, Ross and Mohamed, Zainab and Rigby, Lindsey and Padidela, Raja and Skae, Mars and Mironov, Aleksandr and Starborg, Tobias and Kadler, Karl and Cosgrove, Karen and Banerjee, Indraneel and Dunne, Mark
American Journal of Clinical Pathology, ISSN 0002-9173, 06/2016, Volume 145, Issue 6, pp. 757 - 768
Objectives: To quantify islet cell nucleomegaly in controls and tissues obtained from patients with congenital hyperinsulinism in infancy (CHI) and to examine... 
B cell | Hyperplasia | Islet | Congenital hyperinsulinism | Hypoglycemia | Nucleomegaly | Pancreas | Serial block-face scanning electron microscopy | Insulin | VISUALIZATION | beta cell | MANAGEMENT | BETA-CELLS | PHENOTYPE | PROLIFERATION | MECHANISMS | PATHOLOGY | CHILDREN | POSITRON-EMISSION-TOMOGRAPHY | ABCC8 GENE MUTATION | Congenital Hyperinsulinism - pathology | Islets of Langerhans - pathology | Cell Nucleus - pathology | Humans | Child, Preschool | Female | Infant | Male | Islets of Langerhans - ultrastructure | Cell Nucleus - ultrastructure | Microscopy, Electron | Infant, Newborn | β cell | Original
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12. Full Text The hypoglycemic phenotype is islet cell-autonomous in short-chain hydroxyacyl-CoA dehydrogenase-deficient mice
by Molven, Anders and Hollister-Lock, Jennifer and Hu, Jiang and Martinez, Rachael and Njølstad, Pål R and Liew, Chong Wee and Weir, Gordon and Kulkarni, Rohit N
Diabetes, ISSN 0012-1797, 06/2016, Volume 65, Issue 6, pp. 1672 - 1678
Congenital hyperinsulinism of infancy (CHI) can be caused by inactivating mutations in the gene encoding short-chain 3-hydroxyacyl-CoA dehydrogenase (SCHAD), a... 
CONGENITAL HYPERINSULINISM | OXIDATION | HYPERINSULINEMIC HYPOGLYCEMIA | 3-HYDROXYACYL-COA DEHYDROGENASE | INSULIN-SECRETION | ENDOCRINOLOGY & METABOLISM | BETA-CELL | MUTATIONS | RELEASE | Hypoglycemia - genetics | 3-Hydroxyacyl-CoA Dehydrogenase - deficiency | Hypoglycemia - enzymology | Congenital Hyperinsulinism - enzymology | Male | Mice, Knockout | Insulin - metabolism | Insulin-Secreting Cells - metabolism | Phenotype | Animals | Congenital Hyperinsulinism - genetics | Mice | Glutamate Dehydrogenase - metabolism | Insulin Secretion | Islet Studies
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13. Full Text Liquid fructose in pregnancy exacerbates fructose-induced dyslipidemia in adult female offspring
by Rodríguez, Lourdes and Panadero, María I and Rodrigo, Silvia and Roglans, Núria and Otero, Paola and Álvarez-Millán, Juan J and Laguna, Juan C and Bocos, Carlos
The Journal of Nutritional Biochemistry, ISSN 0955-2863, 06/2016, Volume 32, pp. 115 - 122
Fructose intake from added sugars correlates with the epidemic rise in metabolic syndrome and related events. Nevertheless, consumption of beverages sweetened... 
Pregnancy | Fructokinase | Fructose | Fetal programming | Dyslipidemia | METABOLIC SYNDROME | ALPHA GENE-EXPRESSION | BIOCHEMISTRY & MOLECULAR BIOLOGY | RATS | FATTY-ACIDS | OBESITY | NUTRITION & DIETETICS | INSULIN-RESISTANCE | FRUCTOKINASE EXPRESSION | LIVER | CHREBP | WEIGHT-GAIN | Beverages - adverse effects | Liver - enzymology | Maternal Nutritional Physiological Phenomena | Fatty Acids, Nonesterified - agonists | Non-alcoholic Fatty Liver Disease - etiology | Gene Expression Profiling | Triglycerides - agonists | Adiponectin - agonists | Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - agonists | Non-alcoholic Fatty Liver Disease - blood | Nutritive Sweeteners - adverse effects | Dyslipidemias - blood | Hyperinsulinism - etiology | Fatty Acids, Nonesterified - blood | Female | Dyslipidemias - etiology | Hyperinsulinism - blood | Hyperinsulinism - physiopathology | Hyperinsulinism - metabolism | Glucose - adverse effects | Fructose - adverse effects | Liver - metabolism | Gene Expression Regulation | Fetal Development | Non-alcoholic Fatty Liver Disease - metabolism | Non-alcoholic Fatty Liver Disease - physiopathology | Random Allocation | Rats, Sprague-Dawley | Fructokinases - metabolism | Adiponectin - blood | Animals | Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - genetics | Fructokinases - chemistry | Triglycerides - blood | Dyslipidemias - metabolism | Fructokinases - genetics | Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - metabolism | Dyslipidemias - physiopathology | Pregnant women | Leptin | Protein binding | RNA | Glucose | Dextrose
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14. Full Text Modulation of brain glutamate dehydrogenase as a tool for controlling seizures
by Rasgado, Lourdes A. Vega and Reyes, Guillermo Ceballos and Díaz, Fernando Vega
Acta Pharmaceutica, ISSN 1330-0075, 12/2015, Volume 65, Issue 4, pp. 443 - 452
Glutamate (Glu) is a major excitatory neurotransmitter involved in epilepsy. Glu is synthesized by glutamate dehydrogenase (GDH, E.C. 1.4.1.3) and dysfunction... 
GABA | GDH | antiepileptics | oxygen consumption | glutamate | MOLECULAR TARGETS | DRUGS | HYPERINSULINISM-HYPERAMMONEMIA SYNDROME | PHARMACOLOGY & PHARMACY | EPILEPSY | Seizures - prevention & control | Brain - enzymology | Male | Anticonvulsants - pharmacology | Valproic Acid - pharmacology | Diazepam - pharmacology | Seizures - chemically induced | Seizures - physiopathology | Time Factors | Glutamate Dehydrogenase - antagonists & inhibitors | Phenytoin - pharmacology | Ketoglutaric Acids - metabolism | Glutamate Dehydrogenase - metabolism | Disease Models, Animal | Seizures - enzymology | Oxidation-Reduction | Brain - physiopathology | Enzyme Inhibitors - pharmacology | Oxygen Consumption | Brain - drug effects | Animals | Deamination | Glutamic Acid - metabolism | Mice | Pentylenetetrazole
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15. Full Text The apoB-to-PCSK9 ratio: A new index for metabolic risk in humans
by Wassef, Hanny, PhD and Bissonnette, Simon, MSc and Saint-Pierre, Nathalie, RN, MSc and Lamantia, Valérie, PDT, MSc and Cyr, Yannick, MSc and Chrétien, Michel, MD, MSc and Faraj, May, PDt, PhD
Journal of Clinical Lipidology, ISSN 1933-2874, 2015, Volume 9, Issue 5, pp. 664 - 675
Background Proprotein convertase subtilisin/kexin type 9 (PCSK9) shuttles low-density lipoprotein (LDL) receptors for degradation, thus upregulates LDL plasma... 
Cardiovascular | adipose tissue | low-density lipoproteins | PCSK9 | Apolipoprotein B100 | type II diabetes mellitus | obesity | FAMILIAL HYPERCHOLESTEROLEMIA | LOW-DENSITY-LIPOPROTEIN | OXIDIZED LDL | APOLIPOPROTEIN-B | OBESE WOMEN | PROPROTEIN CONVERTASES | INSULIN-RESISTANCE | PHARMACOLOGY & PHARMACY | GLUCOSE-TOLERANCE | ADIPOSE-TISSUE | Humans | Middle Aged | Insulin Resistance | Metabolic Diseases - epidemiology | Male | Metabolic Diseases - blood | Risk | Apolipoproteins B - blood | Obesity - blood | Hypertriglyceridemia - blood | Chylomicrons - metabolism | Serine Endopeptidases - blood | Adipose Tissue, White - enzymology | Postprandial Period | Female | Proprotein Convertases - blood | Aged | Hyperinsulinism - blood | Lipoprotein Lipase - metabolism | Proprotein Convertase 9
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