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Hepatic Fasting-Induced PPARα Activity Does Not Depend on Essential Fatty Acids
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Regulation of Ketone Body Metabolism and the Role of PPARα

1
Department of Food Biotechnology, Faculty of Food Technology, University of Agriculture, ul. Balicka 122, 30-149 Kraków, Poland
2
Neurological Cancer Research, Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, 1700 Tulane Ave, New Orleans, LA 70112, USA
*
Author to whom correspondence should be addressed.
Academic Editor: Béatrice Desvergne
Int. J. Mol. Sci. 2016, 17(12), 2093; https://doi.org/10.3390/ijms17122093
Received: 23 September 2016 / Revised: 6 December 2016 / Accepted: 7 December 2016 / Published: 13 December 2016
Ketogenesis and ketolysis are central metabolic processes activated during the response to fasting. Ketogenesis is regulated in multiple stages, and a nuclear receptor peroxisome proliferator activated receptor α (PPARα) is one of the key transcription factors taking part in this regulation. PPARα is an important element in the metabolic network, where it participates in signaling driven by the main nutrient sensors, such as AMP-activated protein kinase (AMPK), PPARγ coactivator 1α (PGC-1α), and mammalian (mechanistic) target of rapamycin (mTOR) and induces hormonal mediators, such as fibroblast growth factor 21 (FGF21). This work describes the regulation of ketogenesis and ketolysis in normal and malignant cells and briefly summarizes the positive effects of ketone bodies in various neuropathologic conditions. View Full-Text
Keywords: β hydroxybutyrate; 3-hydroxy-3-methylglytaryl-CoA synthetase 2 (HMGCS2); fenofibrate; melanoma; glioma; fasting β hydroxybutyrate; 3-hydroxy-3-methylglytaryl-CoA synthetase 2 (HMGCS2); fenofibrate; melanoma; glioma; fasting
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MDPI and ACS Style

Grabacka, M.; Pierzchalska, M.; Dean, M.; Reiss, K. Regulation of Ketone Body Metabolism and the Role of PPARα. Int. J. Mol. Sci. 2016, 17, 2093.

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