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
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DISCUSSION

In physical activity, PPARβ/δ acts as a key regulator of fuel metabolism, promoting a shift from glucose to lipid as the main energy substrate. It promotes cellular lipid uptake, activation of fatty acids by fatty acylCoA synthetase and their mitochondrial uptake and β-oxidation. This mechanism decreased glucose oxidation as a consequence, which mimics caloric restriction and physical exercise conditions. Peroxisome proliferator-activated receptors play a regulatory role in preventing metabolic disorders and in muscle adaptation to fasting and physical exercise [10,21-24]. The studies performed in mice showed that activation of PPARβ/δ in skeletal muscle results in enhanced lipid metabolism as an adaptive response to external stimuli such as food availability and prolonged physical activity [2,25-27]. This activation of PPARβ/δ in skeletal muscle enhances lipid use for energy expenditure, which is preferred to glucose and allows glucose to become more available for peripheral organs. Physical exercise enhances PPARD expression, improves cardio-respiratory fitness and decreases circulating lipids levels [13]. In parallel with decreased liver fat accumulation and inflammatory markers, enhanced glucose uptake associated with physical exercise is also observed [11,13]. Moreover, the type and duration of exercise determines muscle mass or hypertrophy [28,29]. In our study, we found significantly increased expression of PPARD after a training cycle of 2 months. Our results are consistent with other authors’ results of research on animals models [30-32]. Mice undergoing endurance exercise showed an accumulation of PPARβ/δ protein in muscle [15]. Further, muscle-specific over expression of PPARD in mice enhanced muscle metabolism (fatty acid in flux and β-oxidation) and remodeled muscle fiber type to increase oxidative type 2a but not type 1 fibers. Those mice also showed decreased body fat mass and thus, had smaller fat cells. Interestingly, PPARD transgenic mice additionally displayed increased glucose metabolism. Together, these results obtained by Luquet et al. [15] in 2003, implicated PPARD in muscle development and adaptive response to exercise training. Another model, a mouse engineered to express a constitutively activated form of PPARβ/δ (VP16- PPARβ/δ) in skeletal muscle, showed that a PPARD-mediated transcriptional pathway can regulate muscle fiber specification, enabling the generation of a strain of mice with a “long-distance running” phenotype [16,33]. As we mentioned above, our study has provided information about training-induced changes in the expression level of the PPARD gene in peripheral blood. It is worth emphasizing that our results are compatible with those obtained for mRNA expression level analyses performed in human skeletal muscle samples [19,34]. Regular physical activity induces desirable changes in plasma levels of HDL and LDL, respectively, and TGs. Physical exercise helps in maintaining lipid homeostasis, enhances glucose uptake and expenditure and also leads to changes in fiber type composition from glycolytic (type II b/x) to slow/fast oxidative (types I and IIa) fibers [35]. Positive effects of exercise are also seen on blood TGs, but little specific effect is seen on LDL and total cholesterol (TC). Abundant evidence supports the benefits of exercise on levels of certain blood lipids (namely HDL-C and TG) [36]. During the 8-week long training cycle we also observed changes in lipid profile, confirming the results of other researchers [37,38]. However, we did not find any statistically significant differences before and after the training cycle. We have also documented that 8-week long training cycles lead to changes in the absolute FAT (kg) level (decreased). The studies of other authors also showed the decrease in absolute FAT (kg) under the influence of physical activity [39,40]. Many researchers showed that PPARβ/δ has been associated with the development of obesity. In mechanism of obesity development, PPARβ/δ activation leads to loss of adipose mass in different mouse models of obesity (stimulating fatty acid oxidation) [33]. Moreover, the same effects on fatty acid oxidation have been observed in heart muscle (improved muscle contraction) [41]. Research suggested that high-fat-diet-induced adiposity was strongly inhibited by activation of PPARβ/δ in adipose tissue. Moreover, in vitro model activation of PPARβ/δ in adipocytes and skeletal muscle cells promotes fatty acid oxidation and utilization. The study showed that PPARβ/δ served as a widespread regulator of fat burning and identified PPARβ/δ as a potential target in treatment of obesity [33]. It is very possible that the expression of this gene may affect the body composition analysis. Our research may provide a starting point for further investigating interactions between PPARD gene expression level and the lipid profile parameters. However, our examination has some limitations caused partly by a small study group and biological material we had at our disposal. Due to the fact that muscle biopsy is an invasive procedure (especially in young people), we did not have the opportunity to directly measure mRNA expression level in skeletal muscles. Additionally, there is only limited knowledge about circadian clock gene regulation by PPARD and about its role in epigenetically modified regulation of skeletal muscle metabolism and function. Ultimately, much work remains to be done before any clinical PPARβ/δ-based interventions will be possible in analysis of body composition in athletes.



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