Reprint

PPARs in Cellular and Whole Body Energy Metabolism

Edited by
January 2019
582 pages
  • ISBN978-3-03897-461-1 (Paperback)
  • ISBN978-3-03897-462-8 (PDF)

This book is a reprint of the Special Issue PPARs in Cellular and Whole Body Energy Metabolism that was published in

Biology & Life Sciences
Chemistry & Materials Science
Medicine & Pharmacology
Summary

At no other time in its history has humankind been as concerned about good health. Lifestyle habits are promoted as indispensable allies for the daily prevention against so-called metabolic diseases. Paradoxically, the world has never been so obese, while the beauty canons have never been so skinny! However, there is more to energy balance than alterations in body weight. In the 1990s, it was found that fatty acids not only function as fuel molecules only, but also serve as signaling molecules. They bind nuclear hormone receptors, the Peroxisome Proliferator-Activated Receptors, commonly referred to by the acronym PPARs. PPARs are transcription factors that directly control the expression of genes of metabolism, thereby impacting a multitude of pathways crucial for whole body physiology. PPARs are also activated by synthetic agonists, which are drugs used for lowering triglycerides and blood sugar. This book features articles that address tools for the identification of novel PPAR ligands, as well as the roles of the receptors in several organs, such as the brain, heart, liver, adipose tissue, gut, and muscle. As such, this book documents the multifaceted roles of these nuclear receptors that continue to attract significant attention, not least because of their still not fully realized potential to treat several health conditions.

Format
  • Paperback
License
© 2019 by the authors; CC BY-NC-ND license
Keywords
PPARγ; intestine; lipid metabolism; peroxisome proliferator-activated receptor α (PPARα); clofibrate; fatty acid β-oxidation; pigs; lysophospholipids; PPARγ; vascular diseases; dementia; spinal cord injury; PPARγ; N-benzylbenzamide derivatives; 3D-QSAR; CoMFA; CoMSIA; molecular docking; exercise; PPAR; SNP; obesity; lipid; glucose; HbA1c; liver enzyme; PPARβ/δ; obesity; dyslipidaemia; type 2 diabetes mellitus; non-alcoholic fatty liver disease; PPARs; energy homeostasis; fatty acid oxidation; glucose-lipid metabolism; metabolic syndrome; PPARs; pemafibrate; elafibrinor; WNT/β-catenin pathway; PPARγ; multiple sclerosis; energy metabolism; aerobic glycolysis; demyelination; Warburg effect; circadian rhythms; clock genes; PPAR; CAR; LXR; obesity; atherosclerosis; peroxisome proliferator-activated receptor; skeletal muscle; lipid metabolism; insulin resistance; aging; physical exercise; type 2 diabetes; muscle regeneration; human performance; aerobic training; genetic predisposition; anaerobic threshold; muscle fibers; glucose tolerance; insulin response; VO2max; VO2peak; mitochondria activity; cholesterol levels; PIMT/NCOA6IP; PRIP/NCOA6; PPARα; dilated cardiomyopathy; cardiac fibrosis; energy metabolism; scavenger receptor; PPAR nuclear receptors; PGC-1; fatty acid oxidation; energy metabolism; GHRP; hexarelin; atherosclerosis; insulin resistance; obesity; type 2 diabetes; atherosclerosis; neurodegenerative disease; inflammation; macrophages; T cells; PPARs; metabolism; gender; multiple sclerosis; metabolism; peroxisome proliferator-activated receptors; immune system; neuroinflammation; neurodegeneration; nuclear receptors; PPARα; PPARγ; PPARβ/δ; post-translational modifications; endothelial cells; vascular endothelial growth factor; Peroxisome proliferator-activated receptor γ; Endothelial Differentiation-related factor 1; stem cells; metabolism; PPARs; PPARβ/δ; NAFLD; NASH; steatosis; liver; lipid metabolism; nuclear receptors; energy metabolism; cancer metabolism; PPARβ/δ; regeneration; proliferation; differentiation; metabolism; Wnt signaling; PDK1; Akt; glycolysis; Skeletal muscle; regeneration; myogenesis; adipogenesis; muscle stem cells; satellite cells; inflammation; PPARg; PPARγ; metabolism; lipid; RAAS; nuclear receptors; kidney; PPAR; metabolism; adipose tissue; obesity; pregnancy; aging; caloric restriction; PPAR; ligand; T2DM; dyslipidemia; TZDs; melanoma; peroxisome proliferator–activated receptor β/δ; migration; EMT; invasion; metastasis; PPAR; agonist; indole; scaffold; tuning; PPAR-δ; β-oxidation metabolism; inflammation; cancer; PGC-1α; metabolic homeostasis; adipose tissue; mitochondria; PPAR agonists; bezafibrate; heart; cardiomyopathy; heart failure; lipids; fatty acid oxidation; energy metabolism; mitochondria; anakoinosis; communicative reprogramming; nuclear transcription factors; metronomic low-dose chemotherapy; glitazones; all-trans retinoic acid; COX-2 inhibitor; master modulators; undruggable targets; therapy pillar; peroxisome proliferator-activated receptors (PPARs); energy homeostasis; metabolic regulations; organ cross-talk; cancer and reprogramming of energy metabolism; systems biology