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Elucidation of Molecular Mechanism of a Selective PPARα Modulator, Pemafibrate, through Combinational Approaches of X-ray Crystallography, Thermodynamic Analysis, and First-Principle Calculations
Open AccessArticle

Effects of Dietary Anaplerotic and Ketogenic Energy Sources on Renal Fatty Acid Oxidation Induced by Clofibrate in Suckling Neonatal Pigs

Laboratory of Developmental Nutrition, Department of Animal Sciences, North Carolina State University, Raleigh, NC 27695, USA
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Author to whom correspondence should be addressed.
Current Address: Sales Department, Zinpro Corporation, Eden Prairie, MN 55344, USA.
Current Address: College of Animal Science and Technology, China Agricultural University, Beijing 100094, China.
§
Current Address: Guangdong Provincial Key Laboratory of Animal Nutrition and Regulation, College of Animal Science, South China Agricultural University, Guangzhou 510000, China.
Current Address: College of Biological Engineering, Henan University of Technology, Zhengzhou 450001, China.
Int. J. Mol. Sci. 2020, 21(3), 726; https://doi.org/10.3390/ijms21030726
Received: 25 November 2019 / Revised: 17 January 2020 / Accepted: 20 January 2020 / Published: 22 January 2020
(This article belongs to the Special Issue PPARs in Metabolic Regulation: Implications for Health and Disease)
Maintaining an active fatty acid metabolism is important for renal growth, development, and health. We evaluated the effects of anaplerotic and ketogenic energy sources on fatty acid oxidation during stimulation with clofibrate, a pharmacologic peroxisome proliferator-activated receptor α (PPARα) agonist. Suckling newborn pigs (n = 72) were assigned into 8 dietary treatments following a 2 × 4 factorial design: ± clofibrate (0.35%) and diets containing 5% of either (1) glycerol-succinate (GlySuc), (2) tri-valerate (TriC5), (3) tri-hexanoate (TriC6), or (4) tri-2-methylpentanoate (Tri2MPA). Pigs were housed individually and fed the iso-caloric milk replacer diets for 5 d. Renal fatty acid oxidation was measured in vitro in fresh tissue homogenates using [1-14C]-labeled palmitic acid. The oxidation was 30% greater in pig received clofibrate and 25% greater (p < 0.05) in pigs fed the TriC6 diet compared to those fed diets with GlySuc, TriC5, and Tri2MPA. Addition of carnitine also stimulated the oxidation by twofold (p < 0.05). The effects of TriC6 and carnitine on palmitic acid oxidation were not altered by clofibrate stimulation. However, renal fatty acid composition was altered by clofibrate and Tri2MPA. In conclusion, modification of anaplerosis or ketogenesis via dietary substrates had no influence on in vitro renal palmitic acid oxidation induced by PPARα activation. View Full-Text
Keywords: Renal fatty acid oxidation; anaplerotic and ketogenic energy; PPARα activation Renal fatty acid oxidation; anaplerotic and ketogenic energy; PPARα activation
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Lin, X.; Pike, B.; Zhao, J.; Fan, Y.; Zhu, Y.; Zhang, Y.; Wang, F.; Odle, J. Effects of Dietary Anaplerotic and Ketogenic Energy Sources on Renal Fatty Acid Oxidation Induced by Clofibrate in Suckling Neonatal Pigs. Int. J. Mol. Sci. 2020, 21, 726.

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