Improved insulin sensitivity after treatment with PPARγ and PPARα ligands is mediated by genetically modulated transcripts

Biochemistry, Genetics and Molecular Biology

• Insulin Sensitivity 100%
• Receptor Agonists 100%
• Fenofibrate 80%
• Single-Nucleotide Polymorphism 60%
• Pioglitazone 60%
• Fatty Acid Metabolism 40%
• Skeletal Muscle 40%
• Glucose Homeostasis 40%
• Antigen Presentation 40%
• Genetics 20%
• Expression Quantitative Trait Loci 20%
• Twin Study 20%
• Gene Expression 20%
• Mitochondrion 20%
• Insulin Signaling 20%
• cAMP Signaling 20%
• Upregulation 20%
• down Regulation 20%
• Genetic Polymorphism 20%
• Glucose Blood Level 20%
• Amino Acid Metabolism 20%
• AMPK Signaling 20%
• Impaired Glucose Tolerance 20%
• Thiazolidinedione 20%
• Acetyl-CoA 20%

Immunology and Microbiology

• Adipose Tissue 100%
• Insulin Sensitivity 100%
• Agonist 83%
• Single Nucleotide Polymorphism 50%
• Insulin 50%
• Fatty Acid Metabolism 33%
• Skeletal Muscle 33%
• Glucose Homeostasis 33%
• Human Tissue 33%
• Antigen Presentation 33%
• Inflammation Response 16%
• Gene Expression 16%
• Mitochondrion 16%
• Upregulation 16%
• Insulin Signaling 16%
• down Regulation 16%
• Glucose Blood Level 16%
• cAMP Signaling 16%
• Amino Acid Metabolism 16%
• AMPK Signaling 16%
• Genetic Polymorphism 16%
• Expression Quantitative Trait Loci 16%
• Muscle 16%
• Acetic Acid Derivative 16%

Pharmacology, Toxicology and Pharmaceutical Science

• Receptor 100%
• Receptor Agonist 62%
• Fenofibrate 50%
• Pioglitazone 37%
• Monotherapy 37%
• Fatty Acid 25%
• Combination Therapy 25%
• Thiazolidinedione 12%
• Acetyl-CoA 12%
• Propanoate 12%
• Twin Study 12%
• Inflammation 12%
• Impaired Glucose Tolerance 12%
• Branched Chain Amino Acid 12%
• Treatment Group 12%