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Open AccessJournal ArticleDOI

PPARδ Agonism Activates Fatty Acid Oxidation via PGC-1α but Does Not Increase Mitochondrial Gene Expression and Function

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TLDR
It is demonstrated that pharmacological activation of PPARδ induces FAO via PGC-1α, however, PPAR δ agonism does not induce mitochondrial gene expression and function.
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This article is published in Journal of Biological Chemistry.The article was published on 2009-07-10 and is currently open access. It has received 128 citations till now. The article focuses on the topics: GW501516 & Peroxisome proliferator-activated receptor delta.

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Citations
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Journal ArticleDOI

PPARs: diverse regulators in energy metabolism and metabolic diseases.

TL;DR: The nuclear receptor PPARs are fundamentally important for energy homeostasis through their distinct yet overlapping functions and tissue distribution, and studies of these receptors have advanced knowledge of the transcriptional basis of energy metabolism.
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In Vivo Correction of COX Deficiency by Activation of the AMPK/PGC-1α Axis

TL;DR: It is demonstrated that double-recombinant animals overexpressing PGC-1α in skeletal muscle on a Surf1 KO background showed robust induction of mitochondrial biogenesis and increase of mitochondrial respiratory chain activities, including COX.
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Regulation of Skeletal Muscle Physiology and Metabolism by Peroxisome Proliferator-Activated Receptor δ

TL;DR: There is increasing evidence that PPARδ is an important regulator of skeletal muscle metabolism, in particular, muscle lipid oxidation, highlighting the potential utility of this isoform as a drug target.
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Mitochondrial Biogenesis through Activation of Nuclear Signaling Proteins

TL;DR: This regulatory network represents a new therapeutic window into the treatment of the wide spectrum of mitochondrial and neurodegenerative diseases characterized by dysregulation of mitochondrial dynamics and bioenergetic deficiencies.
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Coactivators in PPAR-Regulated Gene Expression

TL;DR: Investigations into the role of coactivators in the function of PPARs should strengthen the understanding of the complexities of metabolic diseases associated with energy metabolism.
References
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Journal ArticleDOI

Mechanisms Controlling Mitochondrial Biogenesis and Respiration through the Thermogenic Coactivator PGC-1

TL;DR: PGC-1, a cold-inducible coactivator of nuclear receptors, stimulates mitochondrial biogenesis and respiration in muscle cells through an induction of uncoupling protein 2 (UCP-2) and through regulation of the nuclear respiratory factors (NRFs).
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Transcriptional co-activator PGC-1α drives the formation of slow-twitch muscle fibres

TL;DR: Using fibre-type-specific promoters, it is shown in cultured muscle cells that PGC-1α activates transcription in cooperation with Mef2 proteins and serves as a target for calcineurin signalling, which has been implicated in slow fibre gene expression.
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Differential expression of peroxisome proliferator-activated receptors (PPARs): tissue distribution of PPAR-alpha, -beta, and -gamma in the adult rat

TL;DR: This work presents the expression patterns of the PPAR subtypes in the adult rat, determined by in situ hybridization using specific probes for PPAR-alpha, -beta and -gamma, and by immunohistochemistry using a polyclonal antibody that recognizes the three rat PPar subtypes.
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Mitochondrial Overload and Incomplete Fatty Acid Oxidation Contribute to Skeletal Muscle Insulin Resistance

TL;DR: Target metabolomics finds that obesity-related insulin resistance in skeletal muscle is characterized by excessive beta-oxidation, impaired switching to carbohydrate substrate during the fasted-to-fed transition, and coincident depletion of organic acid intermediates of the tricarboxylic acid cycle.
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