Abstract
The aim of the present work was to study the consequences of chronic exercise training on factors involved in the regulation of mitochondrial remodeling and biogenesis, as well as the ability to produce energy and improve insulin sensitivity and glucose uptake in rat brown adipose tissue (BAT). Male Wistar rats were divided into two groups: (1) control group (C; n = 10) and (2) exercise-trained rats (ET; n = 10) for 8 weeks on a motor treadmill (five times per week for 50 min). Exercise training reduced body weight, plasma insulin, and oxidized LDL concentrations. Protein expression of ATP-independent metalloprotease (OMA1), short optic atrophy 1 (S-OPA1), and dynamin-related protein 1 (DRP1) in BAT increased in trained rats, and long optic atrophy 1 (L-OPA1) and mitofusin 1 (MFN1) expression decreased. BAT expression of nuclear respiratory factor type 1 (NRF1) and mitochondrial transcription factor A (TFAM), the main factors involved in mitochondrial biogenesis, was higher in trained rats compared to controls. Exercise training increased protein expression of sirtuin 1 (SIRT1), peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α) and AMP-activated protein kinase (pAMPK/AMPK ratio) in BAT. In addition, training increased carnitine palmitoyltransferase II (CPT II), mitochondrial F1 ATP synthase α-chain, mitochondrial malate dehydrogenase 2 (mMDH) and uncoupling protein (UCP) 1,2,3 expression in BAT. Moreover, exercise increased insulin receptor (IR) ratio (IRA/IRB ratio), IRA-insulin-like growth factor 1 receptor (IGF-1R) hybrids and p42/44 activation, and decreased IGF-1R expression and IR substrate 1 (p-IRS-1) (S307) indicating higher insulin sensitivity and favoring glucose uptake in BAT in response to chronic exercise training. In summary, the present study indicates that chronic exercise is able to improve the energetic profile of BAT in terms of increased mitochondrial function and insulin sensitivity.
Highlights
Brown adipose tissue (BAT) plays a major role in body energy expenditure and contains numerous mitochondria that function to mediate adaptive thermogenesis and protect against hypothermia and obesity (Cannon and Nedergaard, 2004)
The aim of the present work was to study the consequences of chronic exercise training on factors involved in the regulation of mitochondrial remodeling and biogenesis, as well as the ability to produce energy and improve insulin sensitivity and glucose uptake in rat brown adipose tissue (BAT)
Mitochondrial fission is mediated by dynamin-related protein 1 (Drp1), which is mainly located in the cytosol (Smirnova et al, 2001)
Summary
Brown adipose tissue (BAT) plays a major role in body energy expenditure and contains numerous mitochondria that function to mediate adaptive thermogenesis and protect against hypothermia and obesity (Cannon and Nedergaard, 2004). The ATP-independent metalloprotease OMA1, a proteolytic enzyme located in the inner mitochondrial membrane, is responsible for OPA1 proteolysis (Quiros et al, 2013) Stress conditions, such as the induction of apoptosis and the specific dissipation of mitochondrial membrane potential, induce the cleavage of OPA1 to short isoforms by OMA1, resulting in the inhibition of mitochondrial fusion (Head et al, 2009; Jiang et al, 2014). Nrf interacts with mitochondrial transcription factor A (Tfam), which drives transcription and replication of mitochondrial DNA and, mitochondrial biogenesis (Vina et al, 2009) Both AMP-activated protein kinase (AMPK) and the silent information regulator protein (Sir2) homolog SIRT1 are activators of PGC1α (Fulco and Sartorelli, 2008)
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