scholarly journals Identification and Mechanism of 10-Carbon Fatty Acid as Modulating Ligand of Peroxisome Proliferator-activated Receptors

2011 ◽  
Vol 287 (1) ◽  
pp. 183-195 ◽  
Author(s):  
Raghu R. V. Malapaka ◽  
SokKean Khoo ◽  
Jifeng Zhang ◽  
Jang H. Choi ◽  
X. Edward Zhou ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Peroxisome Proliferator ◽  
Carbon Fatty Acid ◽  
Peroxisome Proliferator Activated Receptors

scholarly journals Metabolic Functions of Peroxisome Proliferator-Activated Receptorβ/δin Skeletal Muscle

PPAR Research ◽  
2007 ◽  
Vol 2007 ◽  
pp. 1-6 ◽  
Author(s):  
Céline Gaudel ◽  
Paul A. Grimaldi
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Environmental Changes ◽  
Dietary Lipids ◽  
Peroxisome Proliferator ◽  
Adaptive Responses ◽  
Insulin Sensitizer ◽  
Metabolic Functions ◽  
Pharmacological Targets ◽  
Peroxisome Proliferator Activated Receptors

Peroxisome proliferator-activated receptors (PPARs) are transcription factors that act as lipid sensors and adapt the metabolic rates of various tissues to the concentration of dietary lipids. PPARs are pharmacological targets for the treatment of metabolic disorders. PPARαand PPARγare activated by hypolipidemic and insulin-sensitizer compounds, such as fibrates and thiazolidinediones. The roles of PPARβ/δin metabolic regulations remained unclear until recently. Treatment of obese monkeys and rodents by specific PPARβ/δagonists promoted normalization of metabolic parameters and reduction of adiposity. Recent evidences strongly suggested that some of these beneficial actions are related to activation of fatty acid catabolism in skeletal muscle and also that PPARβ/δis involved in the adaptive responses of skeletal muscle to environmental changes, such as long-term fasting or physical exercise, by controlling the number of oxidative myofibers. These observations indicated that PPARβ/δagonists might have therapeutic usefulness in metabolic syndrome by increasing fatty acid consumption in skeletal muscle and reducing obesity.

scholarly journals Selective Cooperation between Fatty Acid Binding Proteins and Peroxisome Proliferator-Activated Receptors in Regulating Transcription

2002 ◽  
Vol 22 (14) ◽  
pp. 5114-5127 ◽  
Author(s):  
Nguan-Soon Tan ◽  
Natacha S. Shaw ◽  
Nicolas Vinckenbosch ◽  
Peng Liu ◽  
Rubina Yasmin ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Fatty Acid ◽  
Binding Proteins ◽  
Lipid Binding ◽  
Fatty Acid Binding Proteins ◽  
Peroxisome Proliferator ◽  
Fatty Acid Binding ◽  
Peroxisome Proliferator Activated Receptors ◽  
Retinoic Acid Binding Proteins ◽  
Crabp Ii

ABSTRACT Lipophilic compounds such as retinoic acid and long-chain fatty acids regulate gene transcription by activating nuclear receptors such as retinoic acid receptors (RARs) and peroxisome proliferator-activated receptors (PPARs). These compounds also bind in cells to members of the family of intracellular lipid binding proteins, which includes cellular retinoic acid-binding proteins (CRABPs) and fatty acid binding proteins (FABPs). We previously reported that CRABP-II enhances the transcriptional activity of RAR by directly targeting retinoic acid to the receptor. Here, potential functional cooperation between FABPs and PPARs in regulating the transcriptional activities of their common ligands was investigated. We show that adipocyte FABP and keratinocyte FABP (A-FABP and K-FABP, respectively) selectively enhance the activities of PPARγ and PPARβ, respectively, and that these FABPs massively relocate to the nucleus in response to selective ligands for the PPAR isotype which they activate. We show further that A-FABP and K-FABP interact directly with PPARγ and PPARβ and that they do so in a receptor- and ligand-selective manner. Finally, the data demonstrate that the presence of high levels of K-FABP in keratinocytes is essential for PPARβ-mediated induction of differentiation of these cells. Taken together, the data establish that A-FABP and K-FABP govern the transcriptional activities of their ligands by targeting them to cognate PPARs in the nucleus, thereby enabling PPARs to exert their biological functions.

scholarly journals HDAC Inhibition Modulates Cardiac PPARs and Fatty Acid Metabolism in Diabetic Cardiomyopathy

PPAR Research ◽  
2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Ting-I Lee ◽  
Yu-Hsun Kao ◽  
Wen-Chin Tsai ◽  
Cheng-Chih Chung ◽  
Yao-Chang Chen ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Hdac Inhibitor ◽  
Acid Metabolism ◽  
Adenosine Monophosphate ◽  
Left Ventricular ◽  
Peroxisome Proliferator ◽  
Hdac Inhibition ◽  
Glucose Levels ◽  
Peroxisome Proliferator Activated Receptors

Peroxisome proliferator-activated receptors (PPARs) regulate cardiac glucose and lipid homeostasis. Histone deacetylase (HDAC) inhibitor has anti-inflammatory effects which may play a key role in modulating PPARs and fatty acid metabolism. The aim of this study was to investigate whether HDAC inhibitor, MPT0E014, can modulate myocardial PPARs, inflammation, and fatty acid metabolism in diabetes mellitus (DM) cardiomyopathy. Electrocardiography, echocardiography, and western blotting were used to evaluate the electrophysiological activity, cardiac structure, fatty acid metabolism, inflammation, and PPAR isoform expressions in the control and streptozotocin-nicotinamide-induced DM rats with or without MPT0E014. Compared to control, DM and MPT0E014-treated DM rats had elevated blood glucose levels and lower body weights. However, MPT0E014-treated DM and control rats had smaller left ventricular end-diastolic diameter and shorter QT interval than DM rats. The control and MPT0E014-treated DM rats had greater cardiac PPAR-αand PPAR-δprotein expressions, but less cardiac PPAR-γthan DM rats. Moreover, control and MPT0E014-treated DM rats had lower concentrations of 5′ adenosine monophosphate-activated protein kinase 2α, PPAR-γcoactivator 1α, phosphorylated acetyl CoA carboxylase, cluster of differentiation 36, diacylglycerol acyltransferase 1 (DGAT1), DGAT2, tumor necrosis factor-α, and interleukin-6 protein than DM rats. HDAC inhibition significantly attenuated DM cardiomyopathy through modulation of cardiac PPARS, fatty acid metabolism, and proinflammatory cytokines.

Sign in / Sign up

Export Citation Format

Share Document