scholarly journals Long-term effects of peroxisome proliferator-activated receptor ligand bezafibrate on N-terminal pro-B type natriuretic peptide in patients with advanced functional capacity impairment

2009 ◽  
Vol 8 (1) ◽  
pp. 5 ◽  
Author(s):  
Koichi Node ◽  
Teruo Inoue ◽  
Valentin Boyko ◽  
Ilan Goldberg ◽  
Enrique Z Fisman ◽  
...  
Keyword(s):  
Natriuretic Peptide ◽  
Functional Capacity ◽  
Peroxisome Proliferator ◽  
Long Term Effects ◽  
Receptor Ligand ◽  
Peroxisome Proliferator Activated Receptor

scholarly journals Maternal folic acid consumption during gestation and its long-term effects on offspring's liver: a systematic review

2017 ◽  
Vol 17 (1) ◽  
pp. 7-15 ◽  
Author(s):  
Flavia Bittencourt Brasil ◽  
Luiz Henrique Amarante ◽  
Marcos Roberto de Oliveira
Keyword(s):  
Systematic Review ◽  
Folic Acid ◽  
Medical Society ◽  
Peroxisome Proliferator ◽  
Long Term Effects ◽  
High Intake ◽  
Peroxisome Proliferator Activated Receptor ◽  
Acid Consumption ◽  
Maternal Supplementation

Abstract Objectives: describing the effects of maternal supplementation with folic acid (FA) exclusively during gestation on offspring's liver at later stages in life. Supplementation with FA during gestation has been recommended by the medical society worldwide. The liver has a central role on the substances of metabolism and homeostasis and some studies have shown that a high intake of FA at other periods in life may cause hepatic damage. Methods: a systematic review through which the following databases were consulted: Medline, through platforms of Pubmed, Lilacs and Scielo. The research was performed by keywords such as: "Folic acid", "Gestation", "Rat", "Offspring" and "Liver". Articles which evaluate the effect of FA consumption during both gestation and lactation were excluded. Results: FA consumption avoids disorders on expression of peroxisome proliferator-activated receptor alpha (PPARα) and glucocorticoid receptor (GccR), its lack did not change enzyme activity of the male offspring's liver in adulthood. Supplementation with FA during gestation did not change iron hepatic levels or lipid composition, but had an antioxidant effect on it. Conclusions: supplementation with FA at recommended doses did not cause toxic effects and is very likely to avoid deleterious effects in the liver of the offspring regarding the epigenetic level.

scholarly journals Peroxisome Proliferator-Activated Receptor α (PPARα) Potentiates, whereas PPARγ Attenuates, Glucose-Stimulated Insulin Secretion in Pancreatic β-Cells

Endocrinology ◽  
2005 ◽  
Vol 146 (8) ◽  
pp. 3266-3276 ◽  
Author(s):  
Kim Ravnskjaer ◽  
Michael Boergesen ◽  
Blanca Rubi ◽  
Jan K. Larsen ◽  
Tina Nielsen ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Mitochondrial Membrane ◽  
Uncoupling Protein ◽  
Peroxisome Proliferator ◽  
Dependent Manner ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Peroxisome Proliferator Activated Receptor ◽  
Glucose Stimulated Insulin Secretion

Abstract Fatty acids (FAs) are known to be important regulators of insulin secretion from pancreatic β-cells. FA-coenzyme A esters have been shown to directly stimulate the secretion process, whereas long-term exposure of β-cells to FAs compromises glucose-stimulated insulin secretion (GSIS) by mechanisms unknown to date. It has been speculated that some of these long-term effects are mediated by members of the peroxisome proliferator-activated receptor (PPAR) family via an induction of uncoupling protein-2 (UCP2). In this study we show that adenoviral coexpression of PPARα and retinoid X receptor α (RXRα) in INS-1E β-cells synergistically and in a dose- and ligand-dependent manner increases the expression of known PPARα target genes and enhances FA uptake and β-oxidation. In contrast, ectopic expression of PPARγ/RXRα increases FA uptake and deposition as triacylglycerides. Although the expression of PPARα/RXRα leads to the induction of UCP2 mRNA and protein, this is not accompanied by reduced hyperpolarization of the mitochondrial membrane, indicating that under these conditions, increased UCP2 expression is insufficient for dissipation of the mitochondrial proton gradient. Importantly, whereas expression of PPARγ/RXRα attenuates GSIS, the expression of PPARα/RXRα potentiates GSIS in rat islets and INS-1E cells without affecting the mitochondrial membrane potential. These results show a strong subtype specificity of the two PPAR subtypes α and γ on lipid partitioning and insulin secretion when systematically compared in a β-cell context.

scholarly journals Muscle PGC-1α is required for long-term systemic and local adaptations to a ketogenic diet in mice

2017 ◽  
Vol 312 (5) ◽  
pp. E437-E446 ◽  
Author(s):  
Svenia Schnyder ◽  
Kristoffer Svensson ◽  
Bettina Cardel ◽  
Christoph Handschin
Keyword(s):  
Skeletal Muscle ◽  
Weight Control ◽  
Physiological Adaptation ◽  
Acid Oxidation ◽  
Peroxisome Proliferator ◽  
Dependent Manner ◽  
Dietary Interventions ◽  
Peroxisome Proliferator Activated Receptor ◽  
Local Adaptations

Low-carbohydrate/high-fat (LCHF) diets are increasingly popular dietary interventions for body weight control and as treatment for different pathological conditions. However, the mechanisms of action are still poorly understood, in particular, in long-term administration. Besides liver, brain, and heart, skeletal muscle is one of the major organs involved in the regulation of physiological and pathophysiological ketosis. We assessed the role of the peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) in skeletal muscle of male wild-type control and PGC-1α muscle-specific knockout mice upon 12 wk of LCHF diet feeding. Interestingly, LCHF diet administration increased oxygen consumption in a muscle PGC-1α-dependent manner, concomitant with a blunted transcriptional induction of genes involved in fatty acid oxidation and impairment in exercise performance. These data reveal a new role for muscle PGC-1α in regulating the physiological adaptation to long-term LCHF diet administration.

scholarly journals How Epigenetic Modifications Drive the Expression and Mediate the Action of PGC-1α in the Regulation of Metabolism

2019 ◽  
Vol 20 (21) ◽  
pp. 5449 ◽  
Author(s):  
Anne I. Krämer ◽  
Christoph Handschin
Keyword(s):  
Current Knowledge ◽  
Transcriptional Networks ◽  
Peroxisome Proliferator ◽  
Epigenetic Mechanisms ◽  
Epigenetic Changes ◽  
Peroxisome Proliferator Activated Receptor ◽  
Regulation Of Metabolism ◽  
Health And Disease ◽  
Short And Long Term

Epigenetic changes are a hallmark of short- and long-term transcriptional regulation, and hence instrumental in the control of cellular identity and plasticity. Epigenetic mechanisms leading to changes in chromatin structure, accessibility for recruitment of transcriptional complexes, and interaction of enhancers and promoters all contribute to acute and chronic adaptations of cells, tissues and organs to internal and external perturbations. Similarly, the peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is activated by stimuli that alter the cellular energetic demand, and subsequently controls complex transcriptional networks responsible for cellular plasticity. It thus is of no surprise that PGC-1α is under the control of epigenetic mechanisms, and constitutes a mediator of epigenetic changes in various tissues and contexts. In this review, we summarize the current knowledge of the link between epigenetics and PGC-1α in health and disease.

Isolation of Human Oral Keratinocyte Progenitor/Stem Cells

2007 ◽  
Vol 86 (4) ◽  
pp. 341-346 ◽  
Author(s):  
K. Izumi ◽  
T. Tobita ◽  
S.E. Feinberg
Keyword(s):  
Stem Cells ◽  
Cell Population ◽  
Proliferative Potential ◽  
Peroxisome Proliferator ◽  
Oral Keratinocytes ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ability To Regenerate ◽  
Forming Efficiency ◽  
Stem Cell Populations

Progenitor/stem cell populations of epithelium are known to reside in the small-sized cell population. Our objective was to physically isolate and characterize an oral keratinocyte-enriched population of small-sized progenitor/stem cells. Primary human oral mucosal keratinocytes cultured in a chemically defined serum-free culture system, devoid of animal-derived feeder cells, were sorted by relative cell size and characterized by immunolabeling for β1 integrin, nuclear transcription factor, peroxisome proliferator-activated receptor-gamma, and cell-cycle analysis. Sorted cells were distinguished as progenitor/stem cells by functional assays and their ability to regenerate an oral mucosal graft. Small-sized cells demonstrated the lowest expression of peroxisome proliferator-activated receptor-gamma, the highest colony-forming efficiency, a longer long-term proliferative potential, an enriched quiescent cell population, and the ability to regenerate an oral mucosal graft, implying that the small-sized cultured oral keratinocytes contained an enriched population of progenitor/stem cells.

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