Mitochondrial biogenesis and PGC‐1α gene expression in male broilers from ascites‐susceptible and ‐resistant lines

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Mitochondria are the major site of oxygen consumption and, as the powerhouses of the cell, are major contributors to oxidative stress (Cawthon, Beers, & Bottje, 2001). Broilers with pulmonary hypertension syndrome suffer from increased oxidative stress and defects in liver and lung mitochondrial oxygen consumption (Cawthon et al., 2001; Iqbal, Cawthon, Wideman, & Bottje, 2001). Research on the aetiology of ascites has focused on cellular damage caused by reactive oxygen species (ROS) (Akşit, Altan, Karul, Balkaya, & Özdemir, 2008). Environmental stressors (such as exercise, cold exposure, caloric restriction and oxidative stress, cell division, renewal and differentiation) might affect the growth and division of pre‐existing mitochondria (mitochondrial biogenesis) within cells (Austin & St‐Pierre, 2012; Ventura‐Clapier, Garnier, & Veksler, 2008). Mitochondria biogenesis can produce variations in mitochondrial size, number and mass (Ventura‐Clapier et al., 2008). Mitochondrial biogenesis might have an impact on cellular oxygen consumption and accordingly oxidative stress. Oxidative stress occurs when the rate of generation of reactive oxygen and nitrogen species exceeds the antioxidant capacity (Akşit et al., 2008).
Peroxisome proliferator‐activated receptor‐γ (PPARγ) coactivator‐1α (PGC‐1α) is the key regulator of mitochondrial biogenesis (Austin & St‐Pierre, 2012; Ueda, Watanabe, Sato, Akiba, & Toyomizu, 2005; Ventura‐Clapier et al., 2008). PGC‐1α coactivates transcription factors, such as nuclear hormone receptors, which control transcription of genes for enzymes involved in metabolic pathways and mitochondrial biogenesis (Walter & Seebacher, 2007). PGC‐1α is also a powerful regulator of energy metabolism (Liang & Ward, 2006). A central function of PGC‐1α that is intimately linked to mitochondrial biogenesis is regulating the expression of numerous ROS‐detoxifying enzymes. Therefore, PGC‐1α simultaneously increases mitochondrial function and minimizes the build‐up of metabolic by‐products, ensuring a global positive impact on oxidative metabolism (Austin & St‐Pierre, 2012).
Genetic, metabolic and dietary factors could influence mitochondrial biogenesis, with direct effects on health and disease (Medeiros, 2008). Thyroid hormone, nitric oxide synthase (NOS/cGMP) and β‐adrenergic stimulation (β/cAMP) have been shown to regulate expression and/or activity of PGC‐1α (Ventura‐Clapier et al., 2008). Strong relationship exists between serum thyroid hormone level and ascites incidence (susceptibility) in broiler chicks from six different commercial strains (Azizian, Rahimi, Kamali, Karimi Torshizi, & Zobdeh, 2013). In addition, fast‐growing breeder sires that are more susceptible to ascites had lower thyroid hormone level compared with ascites‐resistant slow‐growing breeder sires (Malan et al., 2003).
Anthony and colleagues used divergent selection in a commercial broiler line to develop ascites‐susceptible (SUS) and ascites‐resistant (RES) lines (Pavlidis et al., 2007; Wideman, Rhoads, Erf, & Anthony, 2013). We therefore sought to explore the relationship between mitochondrial biogenesis and PGC‐1α gene expression in these two broiler lines.
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