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1. Full Text Angiopoietin-like 4 (ANGPTL4, Fasting-induced Adipose Factor) Is a Direct Glucocorticoid Receptor Target and Participates in Glucocorticoid-regulated Triglyceride Metabolism
by Suneil K. Koliwad and Taiyi Kuo and Lauren E. Shipp and Nora E. Gray and Fredrik Backhed and Alex Yick-Lun So and Robert V. Farese, Jr and Jen-Chywan Wang and Sahlgrenska akademin and Institute of Medicine, Department of Molecular and Clinical Medicine and Institutionen för medicin, avdelningen för molekylär och klinisk medicin and Göteborgs universitet and Gothenburg University and Sahlgrenska Academy
Journal of Biological Chemistry, ISSN 0021-9258, 09/2009, Volume 284, Issue 38, pp. 25593 - 25601
Glucocorticoids are important regulators of lipid homeostasis, and chronically elevated glucocorticoid levels induce hypertriglyceridemia, hepatic steatosis,... 
OBESITY | PLASMA | GENE | CHROMATIN | ANGIOGENESIS | DIET | BIOCHEMISTRY & MOLECULAR BIOLOGY | HYPERLIPIDEMIA | MICE | TRANSCRIPTIONAL REGULATION | PROTEIN-4 | Transcription, Genetic - drug effects | Hypertriglyceridemia - genetics | Humans | Dexamethasone - adverse effects | Receptors, Glucocorticoid - metabolism | Hepatocytes - metabolism | Fatty Liver - chemically induced | Adipose Tissue - metabolism | Angiopoietin-like 4 Protein | Dexamethasone - pharmacology | Glucocorticoids - genetics | Glucocorticoids - metabolism | Response Elements - genetics | Lipoprotein Lipase - metabolism | Glucocorticoids - adverse effects | Fatty Liver - genetics | Angiopoietins - metabolism | Fatty Liver - metabolism | Lipoprotein Lipase - genetics | Liver - metabolism | Rats | Hypertriglyceridemia - metabolism | Mice, Knockout | Triglycerides - metabolism | Adipose Tissue, White | Hypertriglyceridemia - chemically induced | Animals | Receptors, Glucocorticoid - genetics | Cell Line, Tumor | Dexamethasone - metabolism | Glucocorticoids - pharmacology | Mice | Transcription, Genetic - genetics | Triglycerides - genetics | Angiopoietins - genetics | Index Medicus | Lipids and Lipoproteins | Metabolism, Regulation, and Signaling | Transcription | Dermatologi och venereologi | Dermatology and Venereal Diseases | Dexamethasone/adverse effects/metabolism/pharmacology | Hypertriglyceridemia/chemically induced/genetics/metabolism | Receptors | Adipose Tissue/metabolism | Liver/metabolism | Tumor | Adipose Tissue | Cell Line | Fatty Liver/chemically induced/genetics/metabolism | Triglycerides/genetics/ metabolism | Response Elements/genetics | Angiopoietins/genetics/ metabolism | Knockout | Lipoprotein Lipase/genetics/metabolism | White | Hepatocytes/metabolism | Genetic/drug effects/genetics | Glucocorticoids/adverse effects/genetics/ metabolism/pharmacology | Glucocorticoid/genetics/ metabolism
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2. Full Text Adiponectin Mediates the Metabolic Effects of FGF21 on Glucose Homeostasis and Insulin Sensitivity in Mice
by Lin, Shaoqiang and Lin, Zhuofeng and Tian, Haishan and Lam, Karen S.L and Hoo, Ruby C.L and Konishi, Morichika and Itoh, Nobuyuki and Wang, Yu and Bornstein, Stefan R and Xu, Aimin and Li, Xiaokun
Cell Metabolism, ISSN 1550-4131, 05/2013, Volume 17, Issue 5, pp. 779 - 789
Fibroblast growth factor 21 (FGF21) is a metabolic hormone with pleiotropic effects on regulating glucose and lipid homeostasis and insulin sensitivity.... 
BETA-KLOTHO | PPAR-ALPHA | OBESITY | LIVER | ENDOCRINOLOGY & METABOLISM | RESISTANCE | POSTTRANSLATIONAL MODIFICATIONS | SECRETION | HYPOADIPONECTINEMIA | EXPRESSION | GROWTH-FACTOR 21 | CELL BIOLOGY | Fatty Liver - metabolism | Oxidation-Reduction | Liver - metabolism | Mice, Inbred C57BL | Homeostasis | Hypertriglyceridemia - metabolism | Male | Muscle, Skeletal - metabolism | MAP Kinase Signaling System | Obesity - metabolism | Hyperglycemia - metabolism | Fibroblast Growth Factors - metabolism | Animals | Energy Metabolism | Insulin Resistance - physiology | Adipocytes - metabolism | Glucose - metabolism | Adiponectin - metabolism | Mice | Fatty Acids - metabolism | Glucose metabolism | Hyperglycemia | Physiological aspects | Muscles | Drugstores | Insulin resistance | Fibroblast growth factors | Universities and colleges | Glucose | Insulin | Dextrose
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3. Full Text The FFA receptor GPR40 links hyperinsulinemia, hepatic steatosis, and impaired glucose homeostasis in mouse
by Steneberg, Pär and Rubins, Nir and Bartoov-Shifman, Reut and Walker, Michael D and Edlund, Helena and Medicinska fakulteten and Umeå centrum för molekylär medicin (UCMM) and Umeå universitet
Cell Metabolism, ISSN 1550-4131, 04/2005, Volume 1, Issue 4, pp. 245 - 258
Obesity is typically associated with elevated levels of free fatty acids (FFAs) and is linked to glucose intolerance and type 2 diabetes. FFAs exert divergent... 
STIMULATED INSULIN-SECRETION | PROTEIN-COUPLED RECEPTOR | FREE FATTY-ACIDS | ENDOCRINOLOGY & METABOLISM | LONG-TERM EXPOSURE | GENE-EXPRESSION | PANCREATIC BETA-CELLS | PPAR-GAMMA | UNCOUPLING PROTEIN-2 | DIET-INDUCED OBESITY | ADIPOSE-TISSUE | CELL BIOLOGY | Glucose Intolerance - metabolism | Hyperinsulinism - metabolism | Glucose Intolerance - genetics | Fatty Liver - metabolism | Hypertriglyceridemia - genetics | Receptors, G-Protein-Coupled - metabolism | Diabetes Mellitus, Type 2 - genetics | Hypertriglyceridemia - metabolism | Diabetes Mellitus, Type 2 - metabolism | Insulin - metabolism | Animals | Diabetes Mellitus, Type 2 - physiopathology | Receptors, G-Protein-Coupled - deficiency | Glucose - physiology | Islets of Langerhans - metabolism | Homeostasis - physiology | Mice | Receptors, G-Protein-Coupled - genetics | Insulin Secretion | Type 2 diabetes | Obesity | Hyperglycemia | Homeostasis | Glucose | Fatty acids | Insulin | Dextrose | Membrane proteins | Fatty Liver/metabolism | Glucose Intolerance/genetics/metabolism | Hypertriglyceridemia/genetics/metabolism | Receptors; G-Protein-Coupled/deficiency/genetics/metabolism | Homeostasis/physiology | Insulin/secretion | Hyperinsulinism/metabolism | Diabetes Mellitus; Type 2/genetics/metabolism/physiopathology | Islets of Langerhans/metabolism | Glucose/physiology
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4. Full Text Apolipoprotein A-V-heparin interactions - Implications for plasma lipoprotein metabolism
by Lookene, A and Beckstead, JA and Nilsson, S and Olivecrona, G and Ryan, RO and Medicinska fakulteten and Fysiologisk kemi and Institutionen för medicinsk biovetenskap and Umeå universitet
JOURNAL OF BIOLOGICAL CHEMISTRY, ISSN 0021-9258, 07/2005, Volume 280, Issue 27, pp. 25383 - 25387
Transgenic and gene disruption experiments in mice have revealed that apolipoprotein (apo) A-V is a potent regulator of plasma triglyceride (TG) levels. To... 
SULFATE PROTEOGLYCANS | GENE | BIOCHEMISTRY & MOLECULAR BIOLOGY | HYDROLYSIS | TRIGLYCERIDES | ACTIVATED RECEPTOR-ALPHA | LIPASE | MICE | HYPERTRIGLYCERIDEMIA | Surface Plasmon Resonance | Apolipoprotein A-V | Heparin - metabolism | Cholesterol, VLDL - metabolism | Sepharose | Apolipoproteins - metabolism | Apolipoproteins A | Humans | Apolipoproteins C - metabolism | Blood Proteins - metabolism | Triglycerides - metabolism | Animals | Chromatography, Affinity | Dimyristoylphosphatidylcholine - metabolism | Apolipoprotein C-III | Cattle | Liposomes - metabolism | Enzyme Activation | In Vitro Techniques | Lipoprotein Lipase - metabolism | Apolipoproteins/metabolism | Apolipoproteins C/metabolism | Heparin/metabolism | Triglycerides/metabolism | Chromatography; Affinity | Lipoprotein Lipase/metabolism | Cholesterol; VLDL/metabolism | Liposomes/metabolism | Dimyristoylphosphatidylcholine/metabolism | Blood Proteins/metabolism
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5. Full Text Triglyceride metabolism in pregnancy
by Ghio, Alessandra and Bertolotto, Alessandra and Resi, Veronica and Volpe, Laura and Di Cianni, Graziano
2011, Advances in Clinical Chemistry, ISBN 0123870429, Volume 55, 21
During pregnancy, complex changes occur in lipid pro?les. From the 12th week of gestation, phospholipids, cholesterol (total, LDL, HDL), and triglycerides (TG)... 
Triglycerides | Preterm birth | Gestational diabetes | Ketogenesis | Preeclampsia | LIPOPROTEIN METABOLISM | LIPID-METABOLISM | RECREATIONAL PHYSICAL-ACTIVITY | POLYUNSATURATED FATTY-ACIDS | MATERNAL SERUM TRIGLYCERIDE | BIRTH-WEIGHT | ARTERY RISK DEVELOPMENT | GESTATIONAL DIABETES-MELLITUS | MEDICAL LABORATORY TECHNOLOGY | CARBOHYDRATE-METABOLISM | ADIPOSE-TISSUE | Cardiovascular Diseases - etiology | Cardiovascular Diseases - metabolism | Diabetes, Gestational - metabolism | Humans | Hypertriglyceridemia - physiopathology | Ketone Bodies - metabolism | Fetus - metabolism | Hypertriglyceridemia - metabolism | Lipid Metabolism | Risk | Maternal-Fetal Exchange - physiology | Cholesterol - metabolism | Triglycerides - metabolism | Placenta - metabolism | Pregnancy | Hypertriglyceridemia - complications | Infant, Premature - metabolism | Fetal Development - physiology | Glucose - metabolism | Female | Infant, Premature, Diseases - metabolism | Pre-Eclampsia - metabolism | Infant, Newborn
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6. Full Text Critical role of Trib1 in differentiation of tissue-resident M2-like macrophages
by Satoh, Takashi and Kidoya, Hiroyasu and Naito, Hisamichi and Yamamoto, Masahiro and Takemura, Naoki and Nakagawa, Katsuhiro and Yoshioka, Yoshichika and Morii, Eiichi and Takakura, Nobuyuki and Takeuchi, Osamu and Akira, Shizuo
Nature, ISSN 0028-0836, 03/2013, Volume 495, Issue 7442, pp. 524 - 528
Macrophages consist of at least two subgroups, M1 and M2 (refs 1-3). Whereas M1 macrophages are proinflammatory and have a central role in host defence against... 
GLUCOSE-HOMEOSTASIS | OBESITY | TRIBBLES HOMOLOG | INSULIN-RESISTANCE | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | MYELOID LEUKEMOGENESIS | POLARIZATION | ASSOCIATION | ALTERNATIVE ACTIVATION | ADIPOSE-TISSUE | Neutrophils - cytology | Protein-Serine-Threonine Kinases - deficiency | CCAAT-Enhancer-Binding Protein-alpha - metabolism | Eosinophils - metabolism | Hypertriglyceridemia - genetics | Cell Count | Ubiquitin - metabolism | Adipose Tissue - cytology | Diet, High-Fat - adverse effects | Male | Intracellular Signaling Peptides and Proteins - metabolism | Lung - cytology | Intracellular Signaling Peptides and Proteins - deficiency | Adipose Tissue - metabolism | Inflammation Mediators - metabolism | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Female | Cell Differentiation | Cytokines - genetics | Intracellular Signaling Peptides and Proteins - genetics | Neutrophils - metabolism | Protein-Serine-Threonine Kinases - metabolism | Protein Structure, Tertiary | Macrophages - classification | Bone Marrow Cells - cytology | Adipose Tissue - pathology | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Cell Cycle Proteins - deficiency | Lipodystrophy - metabolism | Spleen - cytology | Macrophages - cytology | Organ Specificity | Lipolysis | Hypertriglyceridemia - chemically induced | Macrophages - metabolism | Animals | Intracellular Signaling Peptides and Proteins - chemistry | Insulin Resistance - genetics | Lipodystrophy - pathology | Lipodystrophy - chemically induced | Mice | Protein-Serine-Threonine Kinases - chemistry | Eosinophils - cytology | Bone Marrow Cells - metabolism | Proteins | Care and treatment | Metabolic diseases | Cellular signal transduction | Research | Macrophages | Properties | Identification and classification | Testing | Studies | Spleen | Heart attacks | Transplants & implants | Bone marrow | Binding sites | Metabolic disorders | Defects
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7. Full Text A Liver-Enriched Long Non-Coding RNA, lncLSTR, Regulates Systemic Lipid Metabolism in Mice
by Li, Ping and Ruan, Xiangbo and Yang, Ling and Kiesewetter, Kurtis and Zhao, Yi and Luo, Haitao and Chen, Yong and Gucek, Marjan and Zhu, Jun and Cao, Haiming
Cell Metabolism, ISSN 1550-4131, 03/2015, Volume 21, Issue 3, pp. 455 - 467
Long non-coding RNAs (lncRNAs) constitute a significant portion of mammalian genome, yet the physiological importance of lncRNAs is largely unknown. Here, we... 
LIPOPROTEIN | EVOLUTION | DISEASES | C-II DEFICIENCY | ANNOTATION | TRANSCRIPTION | ENDOCRINOLOGY & METABOLISM | MECHANISMS | HYPERTRIGLYCERIDEMIA | EXPRESSION | PREDICTION | CELL BIOLOGY | Steroid 12-alpha-Hydroxylase - metabolism | Hyperlipidemias - blood | Hyperlipidemias - metabolism | Liver - metabolism | Bile Acids and Salts - metabolism | DNA-Binding Proteins - metabolism | Animals | Triglycerides - blood | Apolipoprotein C-II - metabolism | Signal Transduction - physiology | Mice | Lipoprotein Lipase - metabolism | RNA, Long Noncoding - metabolism | Lipid Metabolism - physiology | RNA | Analysis | Liver | Genomics | Cytochrome P-450 | Lipoprotein lipase | Triglycerides | Deoxycholic acid
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8. Full Text The PPARβ/δ Activator GW501516 Prevents the Down-Regulation of AMPK Caused by a High-Fat Diet in Liver and Amplifies the PGC-1α-Lipin 1-PPARα Pathway Leading to Increased Fatty Acid Oxidation
by Barroso, Emma and Rodríguez-Calvo, Ricardo and Serrano-Marco, Lucía and Astudillo, Alma M and Balsinde, Jesús and Palomer, Xavier and Vázquez-Carrera, Manuel
Endocrinology, ISSN 0013-7227, 05/2011, Volume 152, Issue 5, pp. 1848 - 1859
GW501516 amplifies the PGC-1α-lipin 1-PPARα pathway in liver, leading to increased fatty acid oxidation. Metabolic syndrome-associated dyslipidemia is mainly... 
DENSITY LIPOPROTEIN PRODUCTION | SKELETAL-MUSCLE | METABOLIC SYNDROME | GLUCOSE-METABOLISM | ENDOCRINOLOGY & METABOLISM | ALPHA | PROTEIN-KINASE ACTIVATION | RECEPTOR-DELTA | INSULIN SENSITIVITY | EXPRESSION | GENE-TRANSCRIPTION | AMP-Activated Protein Kinases - metabolism | Immunoblotting | PPAR gamma - metabolism | Liver - drug effects | PPAR-beta - agonists | Lipids - blood | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha | Dietary Fats - administration & dosage | Oxidation-Reduction - drug effects | Trans-Activators - genetics | Phosphorylation - drug effects | Nuclear Proteins - genetics | Fatty Acids - metabolism | Receptors, LDL - genetics | Dietary Fats - adverse effects | Glucose Tolerance Test | PPAR-beta - metabolism | Liver - metabolism | Receptors, LDL - metabolism | Hypertriglyceridemia - metabolism | Nuclear Proteins - metabolism | PPAR alpha - genetics | Down-Regulation - drug effects | Reverse Transcriptase Polymerase Chain Reaction | Phosphatidate Phosphatase | Triglycerides - metabolism | Hypertriglyceridemia - prevention & control | Animals | Signal Transduction - drug effects | Hypertriglyceridemia - etiology | PPAR gamma - agonists | Trans-Activators - metabolism | Mice | Thiazoles - pharmacology | Transcription Factors | PPAR alpha - metabolism
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9. Full Text Reduction of liver fructokinase expression and improved hepatic inflammation and metabolism in liquid fructose-fed rats after atorvastatin treatment
by Vilà, Laia and Rebollo, Alba and Ađalsteisson, Gunnar S and Alegret, Marta and Merlos, Manuel and Roglans, Nuria and Laguna, Juan C
Toxicology and Applied Pharmacology, ISSN 0041-008X, 2011, Volume 251, Issue 1, pp. 32 - 40
Consumption of beverages that contain fructose favors the increasing prevalence of metabolic syndrome alterations in humans, including non-alcoholic fatty... 
Fatty acid oxidation | NAFLD | ChREBP | NFκB | NFΚB | PPAR-ALPHA | KAPPA-B ACTIVATION | LIPID-METABOLISM | ELEMENT-BINDING PROTEIN | HYPERTRIGLYCERIDEMIA | DISEASE | FATTY LIVER | PHARMACOLOGY & PHARMACY | TOXICOLOGY | TRANSCRIPTION FACTOR | UP-REGULATION | NF kappa B | CARDIOVASCULAR RISK | Hypertriglyceridemia - drug therapy | Metallothionein - metabolism | Liver - pathology | Phosphorylation | Hepatitis - enzymology | Liver - enzymology | Fatty Liver - pathology | Male | NF-kappa B - metabolism | I-kappa B Proteins - metabolism | Dietary Carbohydrates - metabolism | Fructose - metabolism | Necrosis | Hepatitis - prevention & control | Liver - drug effects | Hepatitis - genetics | Fatty Liver - enzymology | Inflammation Mediators - metabolism | Non-alcoholic Fatty Liver Disease | Lipid Metabolism - genetics | Fatty Acids - metabolism | Heptanoic Acids - pharmacology | Disease Models, Animal | Cyclic AMP-Dependent Protein Kinases - metabolism | Fatty Liver - genetics | Hepatitis - etiology | Oxidation-Reduction | Down-Regulation | Fatty Liver - prevention & control | Rats | Rats, Sprague-Dawley | Fructokinases - metabolism | Triglycerides - metabolism | Gene Expression Regulation - drug effects | Atorvastatin Calcium | Hypertriglyceridemia - enzymology | Pyrroles - pharmacology | Animals | Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology | Hypertriglyceridemia - etiology | Lipid Metabolism - drug effects | Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - metabolism | Fatty Liver - etiology | Liver diseases | Synthesis | Liver | Physiological aspects | Triglycerides | Beverages | Fatty acids | Fructose | Metallothionein | Antilipemic agents | Protein binding | Index Medicus | Enzymes | Transcription factors | Inflammation | Regulatory sequences | Metabolism | Dietary restrictions | reductase | Fatty liver | Molecular modelling | Hypertriglyceridemia | Atorvastatin | Fructokinase | Supplementation | steatosis | Metabolic disorders | PATIENTS | METALLOTHIONEIN | DIGESTIVE SYSTEM | RATS | TRIGLYCERIDES | HISTOLOGY | 60 APPLIED LIFE SCIENCES | FRUCTOSE | GLANDS | METABOLISM | ENZYMES | GENES | ESTERS | CHEMICAL REACTIONS | VERTEBRATES | LIPIDS | MAMMALS | HUMAN POPULATIONS | OXIDATION | TRANSCRIPTION FACTORS | ANIMALS | SACCHARIDES | CATABOLISM | RODENTS | ORGANIC COMPOUNDS | METALLOPROTEINS | INTAKE | ORGANIC ACIDS | POPULATIONS | SYMPTOMS | HEXOSES | KETONES | ORGANS | MONOSACCHARIDES | DISEASES | INGESTION | INFLAMMATION | LIVER | SYNTHESIS | CARBOXYLIC ACIDS | BEVERAGES | PROTEINS | BODY | PATHOLOGICAL CHANGES | CARBOHYDRATES | CONTROL | FOOD
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10. Full Text Caveolin 1 Modulates Aldosterone‐Mediated Pathways of Glucose and Lipid Homeostasis
by Baudrand, Rene and Gupta, Nidhi and Garza, Amanda E and Vaidya, Anand and Leopold, Jane A and Hopkins, Paul N and Jeunemaitre, Xavier and Ferri, Claudio and Romero, Jose R and Williams, Jonathan and Loscalzo, Joseph and Adler, Gail K and Williams, Gordon H and Pojoga, Luminita H
Journal of the American Heart Association, ISSN 2047-9980, 10/2016, Volume 5, Issue 10, p. n/a
Background Overactivation of the aldosterone and mineralocorticoid receptor (MR) pathway is associated with hyperglycemia and dyslipidemia. Caveolin 1 (cav‐1)... 
caveolin 1 | mineralocorticoid receptor | dyslipidemia | insulin resistance | aldosterone | eplerenone | Insulin resistance | Caveolin 1 | Eplerenone | Aldosterone | Mineralocorticoid receptor | Dyslipidemia | METABOLIC SYNDROME | OXIDATIVE STRESS | CAVEOLIN-1-DEFICIENT MICE | CARDIAC & CARDIOVASCULAR SYSTEMS | OXIDANT STRESS | VASCULAR RELAXATION | MINERALOCORTICOID RECEPTOR BLOCKADE | DIETARY-SODIUM | INSULIN-RESISTANCE | ADIPOCYTE DYSFUNCTION | ALDOSE REDUCTASE | Dyslipidemias - genetics | Aldehyde Reductase - genetics | Hypertriglyceridemia - genetics | Resistin - genetics | Receptors, Mineralocorticoid - metabolism | Humans | Middle Aged | Lipoproteins, HDL - metabolism | Homeostasis | Male | RNA, Messenger - metabolism | Young Adult | Adipose Tissue - metabolism | Aldosterone - metabolism | Spironolactone - pharmacology | Mineralocorticoid Receptor Antagonists - pharmacology | Adult | Aldehyde Reductase - metabolism | Female | Lipid Metabolism - genetics | Retinol-Binding Proteins, Plasma - metabolism | Spironolactone - analogs & derivatives | Resistin - metabolism | NADPH Oxidase 4 - genetics | Signal Transduction | Gene Frequency | Liver - metabolism | Caveolin 1 - genetics | Hypertriglyceridemia - metabolism | Cholesterol - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Mice, Knockout | Triglycerides - metabolism | Blood Glucose - drug effects | Insulin - metabolism | NADPH Oxidase 4 - metabolism | Animals | Adolescent | Insulin Resistance - genetics | Dyslipidemias - metabolism | Glucose - metabolism | Aged | Mice | Polymorphism, Single Nucleotide | Retinol-Binding Proteins, Plasma - genetics
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11. Full Text Dietary, physiological, genetic and pathological influences on postprandial lipid metabolism
by Lopez-Miranda, José and Williams, Christine and Lairon, Denis
British Journal of Nutrition, ISSN 0007-1145, 9/2007, Volume 98, Issue 3, pp. 458 - 473
Most of diurnal time is spent in a postprandial state due to successive meal intakes during the day. As long as the meals contain enough fat, a transient... 
Lifestyle conditions | Diet | Coronary heart disease | Gene polymorphism | Postprandial lipaemia | Physiological and pathological factors | FATTY-ACID-BINDING | CORONARY-ARTERY DISEASE | RECEPTOR-RELATED PROTEIN | lifestyle conditions | LOW-DENSITY-LIPOPROTEIN | EUROPEAN ATHEROSCLEROSIS RESEARCH | gene polymorphism | TRIGLYCERIDE-RICH LIPOPROTEINS | physiological and pathological factors | HEALTHY-YOUNG MEN | postprandial lipaemia | APOLIPOPROTEIN-A-IV | NUTRITION & DIETETICS | MIDDLE-AGED MEN | FAMILIAL COMBINED HYPERLIPIDEMIA | coronary heart disease | diet | Dietary Fats - metabolism | Hyperlipidemias - genetics | Life Style | Hypertriglyceridemia - genetics | Atherosclerosis - genetics | Humans | Dietary Fiber - administration & dosage | Dietary Carbohydrates - metabolism | Obesity - genetics | Postprandial Period - physiology | Dietary Proteins - metabolism | Coronary Disease - metabolism | Apolipoproteins - genetics | Dietary Fats - administration & dosage | Lipid Metabolism - genetics | Dietary Carbohydrates - administration & dosage | Hyperlipidemias - metabolism | Apolipoproteins - metabolism | Dietary Fiber - metabolism | Hypertriglyceridemia - metabolism | Atherosclerosis - metabolism | Obesity - metabolism | Polymorphism, Genetic | Coronary Disease - genetics | Postprandial Period - genetics | Lipid Metabolism - physiology
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12. Full Text Selective Hepatic Insulin Resistance, VLDL Overproduction, and Hypertriglyceridemia
by Sparks, Janet D and Sparks, Charles E and Adeli, Khosrow
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 09/2012, Volume 32, Issue 9, pp. 2104 - 2112
Insulin plays a central role in regulating energy metabolism, including hepatic transport of very low-density lipoprotein (VLDL)–associated triglyceride.... 
apolipoproteins | cytokines | insulin resistance | lipoproteins | obesity | TRIGLYCERIDE TRANSFER PROTEIN | MESSENGER-RNA TRANSLATION | FED HAMSTER MODEL | LOW-DENSITY-LIPOPROTEIN | NECROSIS-FACTOR-ALPHA | ENDOPLASMIC-RETICULUM STRESS | TYROSINE-PHOSPHATASE 1B | APOLIPOPROTEIN-B SECRETION | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | NF-KAPPA-B | UBIQUITIN-PROTEASOME PATHWAY | Up-Regulation | Apolipoproteins B - metabolism | Hypertriglyceridemia - genetics | Phosphatidylinositol Phosphates - metabolism | Cytokines - metabolism | Hypertriglyceridemia - immunology | Signal Transduction | Humans | Hypertriglyceridemia - physiopathology | Liver - metabolism | Insulin Resistance | Hypertriglyceridemia - metabolism | Apolipoproteins B - genetics | Lipoproteins, VLDL - biosynthesis | Liver - physiopathology | Insulin - metabolism | Liver - immunology | Animals | Energy Metabolism | Hypertriglyceridemia - etiology | Inflammation Mediators - metabolism | Blood Glucose - metabolism | Phosphatidylinositol 3-Kinase - metabolism
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