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
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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 (2.6±0.6-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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