Liver PPARα is crucial for whole-body fatty acid homeostasis and is protective against NAFLD. - Wikidata - wikimedia - TriplyDB

Liver PPARα is crucial for whole-body fatty acid homeostasis and is protective against NAFLD.

Liver PPARα is crucial for whole-body fatty acid homeostasis and is protective against NAFLD.

http://www.wikidata.org/entity/Q42101410

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Pleiotropic Actions of Peroxisome Proliferator-Activated Receptors (PPARs) in Dysregulated Metabolic Homeostasis, Inflammation and Cancer: Current Evidence and Future Perspectives PPARs in obesity-induced T2DM, dyslipidaemia and NAFLD.SAK-HV Triggered a Short-period Lipid-lowering Biotherapy Based on the Energy Model of Liver Proliferation via a Novel Pathway.Current and upcoming pharmacotherapy for non-alcoholic fatty liver disease.Glucocorticoid receptor-PPARα axis in fetal mouse liver prepares neonates for milk lipid catabolism IL-33 treatment attenuated diet-induced hepatic steatosis but aggravated hepatic fibrosis Hepatic Fasting-Induced PPARα Activity Does Not Depend on Essential Fatty Acids.PPARs and Mitochondrial Metabolism: From NAFLD to HCC.Peroxisome Proliferator-Activated Receptor Modulation during Metabolic Diseases and Cancers: Master and Minions.Current and future pharmacologic treatment of nonalcoholic steatohepatitis.Concise Review: Current Status and Future Directions on Research Related to Nonalcoholic Fatty Liver Disease.A Combination of Leucine, Metformin, and Sildenafil Treats Nonalcoholic Fatty Liver Disease and Steatohepatitis in Mice.Synthetic and natural Peroxisome Proliferator-Activated Receptor (PPAR) agonists as candidates for the therapy of the metabolic syndrome.Nutrient-sensing nuclear receptors PPARα and FXR control liver energy balance.Distinct but complementary contributions of PPAR isotypes to energy homeostasis.From chronic overnutrition to metaflammation and insulin resistance: adipose tissue and liver contributions.Early gestational maternal low-protein diet diminishes hepatic response to fasting in young adult male mice.White-to-brite conversion in human adipocytes promotes metabolic reprogramming towards fatty acid anabolic and catabolic pathways.Effects of soy isoflavone on hepatic steatosis in high fat-induced rats.CREB3L3 controls fatty acid oxidation and ketogenesis in synergy with PPARα.A Specific ChREBP and PPARα Cross-Talk Is Required for the Glucose-Mediated FGF21 Response.Treatment options for alcoholic and non-alcoholic fatty liver disease: A review.A polyphenol-rich cranberry extract reverses insulin resistance and hepatic steatosis independently of body weight loss.Current and emerging pharmacological therapy for non-alcoholic fatty liver disease.Mice with hyperbilirubinemia due to Gilbert's syndrome polymorphism are resistant to hepatic steatosis by decreased serine 73 phosphorylation of PPARα.Glucocorticoid Receptor β Induces Hepatic Steatosis by Augmenting Inflammation and Inhibition of the Peroxisome Proliferator-activated Receptor (PPAR) α.Amelioration of diet-induced steatohepatitis in mice following combined therapy with ASO-Fsp27 and fenofibrate.Fenofibrate Decreases Insulin Clearance and Insulin Secretion to Maintain Insulin Sensitivity.Caffeine affects HFD-induced hepatic steatosis by multifactorial intervention.Metabolic adaptation to intermittent fasting is independent of peroxisome proliferator-activated receptor alpha.Identification and Characterization of Fenofibrate-Induced Liver Injury.Intermittent Fasting Promotes White Adipose Browning and Decreases Obesity by Shaping the Gut Microbiota.Triglyceride Metabolism in the Liver.Hepatic PPARα function is controlled by polyubiquitination and proteasome-mediated degradation via the coordinated actions of PAQR3 and HUWE1.Acyl-CoA Thioesterase 1 (ACOT1) Regulates PPARα to Couple Fatty Acid Flux With Oxidative Capacity During Fasting.Dual PPARα/γ agonist saroglitazar improves liver histopathology and biochemistry in experimental NASH models.The Peroxisome Proliferator-Activated Receptor α is dispensable for cold-induced adipose tissue browning in mice.Lipidized prolactin-releasing peptide improved glucose tolerance in metabolic syndrome: Koletsky and spontaneously hypertensive rat study.Impairment of PPARα and the Fatty Acid Oxidation Pathway Aggravates Renal Fibrosis during Aging.Endocrine Disruptors and Developmental Origins of Nonalcoholic Fatty Liver Disease.

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P2860

Liver PPARα is crucial for whole-body fatty acid homeostasis and is protective against NAFLD.

http://www.wikidata.org/entity/Q42101410

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2016 nî lūn-bûn

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P2860

Bioconductor: open software development for computational biology and bioinformatics

Peroxisome proliferator-activated receptor alpha-isoform deficiency leads to progressive dyslipidemia with sexually dimorphic obesity and steatosis

Peroxisome proliferator-activated receptor alpha mediates the adaptive response to fasting

Integrated physiology and systems biology of PPARα

Targeted disruption of the alpha isoform of the peroxisome proliferator-activated receptor gene in mice results in abolishment of the pleiotropic effects of peroxisome proliferators

Identification of a physiologically relevant endogenous ligand for PPARalpha in liver

Inventing new medicines: The FGF21 story

Differential expression of peroxisome proliferator-activated receptors (PPARs): tissue distribution of PPAR-alpha, -beta, and -gamma in the adult rat

PPARalpha governs glycerol metabolism

Altered lipid metabolism in residual white adipose tissues of Bscl2 deficient mice

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