ANALYSIS OF THE PPARD GENE EXPRESSION LEVEL CHANGES IN FOOTBALL PLAYERS IN RESPONSE TO THE TRAINING CYCLE
Domańska-Senderowska D, Snochowska A, Szmigielska P, Jastrzębski Z, Jegier A, Kiszałkiewicz J, Dróbka K, Jastrzębska J, Pastuszak-Lewandoska D, Cięszczyk P, Maciejewska-Skrendo A, Zmijewski P, Brzeziańska-Lasota E
*Corresponding Author: Piotr Zmijewski, Ph.D., Faculty of Medicine, University of Information Technology and Management in Rzeszow, Rzeszow, Poland. Tel: +48-22-384-08-12. Fax: +48-22-835-09-77. E-mail: zmijewski@op.pl
page: 19

INTRODUCTION

The peroxisome proliferator-activated receptor (PPAR) belongs to a ligand-dependent family that comprises three subtypes: PPARα, PPARγ and PPARβ/δ, each of which is related to different tissues or cells. In the present study, we examined the PPARD gene, located on the short arm of the chromosome 6 (6p21.1-p21.2), that encodes a member of the PPAR family. This transcription factor gene encompasses an 85 kb section of DNA and consists of nine exons and eight introns [1]. The highest expression level of PPARD mRNA is observed in Sertoli cells, intestine, heart, liver, brain and kidney tissues [2-5]. The most popular ligands of PPARβ/δ are: unsaturated fatty free acid (FFA) and their metabolites [1,2,5,6], GW0742 [7-9], ezetimibe [7], GW501516 [6,10], 15-HETE, 4-HNE, 4-HDDE and ATRA [2]. The PPAR activation plays a vital role in regulation of many physiological and pathological processes, such as energy consumption, inflammation, tissue repair, proliferation and differentiation of various types of cells [1-3]. Mammalian skeletal muscles are a major site of fatty acid catabolism in the fasting state. Thus, factors affecting this process, such as PPARβ/δ, modulate homeostasis at the whole-body level [11,12]. The PPARβ/δ receptor exerts a pleiotropic impact on skeletal muscle physiology and metabolism. The use of cell cultures and animal models has revealed that PPARβ/δ activation results in a metabolic shift promoting lipid utilization (increased fatty acid uptake and oxidation) and reduced carbohydrate oxidation [6,11,13]. These modifications occur through upregulation of the expression of proteins implicated in myocyte energetic substrate preference, such as fat tissue (FAT )/CD36 [13,14], lipoprotein lipase, PDK4 or CPT1 [2,4,6,14]. The PPARβ/δ also promotes mitochondrial biogenesis, angiogenesis and changes in fiber type composition from glycolytic to slow/fast oxidative fibers [11,13,15,16]. Moreover, mice fed with a high fat diet and treated with PPAR agonist showed decreased progress of obesity as well as upgraded glucose tolerance and insulin sensitivity [2,17]. Nutritional status and physical activity are wellknown causative agents of alteration in PPARD expression level in skeletal muscle [2,12,18]. Analysis of the mRNA expression in skeletal muscles obtained from males proved that during recovery from endurance exercise (in the first 3 hours) it can be observed in transient elevated PPARD expression level (2.60.6-fold) [19]. Therefore, we performed this study to evaluate if there is any relationship between training-induced changes in PPARD gene expression level and lipid metabolism parameters.



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