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  • We also investigated fat depots in mesenteric and retroperit


    We also investigated fat depots in mesenteric and retroperitoneal adipose tissues as well as in the liver and verified a reduction in lipid droplets following exercise or exercise and FS oil treatments in the liver from obese mice. Potential molecular candidates in the modulation of adipose tissue by exercise include irisin, which is secreted upon muscle contraction and can change the profile of adipose tissues among other functions [47]. However, a reduced adipose tissue mass in either humans or animals after chronic exercise exposure is mainly attributed to the increase energy expenditure [48]. FS oil treatment did not lead to a reduced fat mass profile in our study, although this has previously been observed elsewhere with other studies demonstrating a reduction in fat storage and the number and size of adipocytes [4], [7], [43]. Here, we believe that the period of treatment (4 weeks) and our mild dose of FS oil were perhaps insufficient to change the fat depots in either liver or adipose tissue, and an extended treatment period as suggested by Baranowski et al. [43] might be required. In our final experiment, we unexpectedly demonstrated that animals treated with FS oil had an increased performance in the incremental load test. Previous studies have been somewhat inconsistent in showing a beneficial effect of ω3 in this area, with no improvement observed in maximal aerobic power, N1-Methylpseudouridine australia threshold or running performance in well-trained soccer players supplemented for 10 weeks with 2.64 g of ω3 (1.6 g of EPA plus 1.04 g DHA) [49]. However, improvements in neuromuscular function, maximal voluntary isometric contractions, performance and fatigue levels were observed elsewhere in athletes after supplementation with 1.1 g of ω3 (375 mg EPA, 230 mg docosapentaenoic acid, 510 mg DHA) [50]. The translation of the current supplementation model to the human application is reasonable, once the ω3 (ALA) adequate intake is 1.6 g/day [51], which could be achievable with 3 mL of FS oil or 7 g of flaxseed.
    Introduction Nonalcoholic steatohepatitis (NASH) is recognized worldwide as a common underlying pathology of chronic liver disease (Ludwig et al., 1980, Marrero et al., 2002). This condition is associated with increased liver-related mortality and may result in hepatocellular carcinoma, even in the absence of cirrhosis (Vernon et al., 2011, Machado and Diehl, 2016). At the present time, there is no approved therapy for NASH (Rinella, 2015, Lassailly et al., 2016). Although a “two-hit” theory was previously accepted as a pathogenetic mechanism of NASH (Day and James, 1998), a better model, the “multiple-hits hypothesis,” was recently proposed, in which several disease-promoting factors occur concurrently rather than consecutively (Tilg and Moschen, 2010). Recent reports have indicated impaired bioavailability of liver n−6 and n−3 long-chain polyunsaturated fatty acids (PUFAs) in nonalcoholic fatty liver disease (NAFLD), including NASH (Araya et al., 2004, Videla et al., 2004, Puri et al., 2007, Puri et al., 2009). In particular, NAFLD and NASH associated with obesity have been linked to the depletion of hepatic n−3 long-chain PUFAs. The n−6/n−3 PUFAs ratio in both steatosis and steatohepatitis patients was shown to be higher than that in healthy individuals (Araya et al., 2004, Arendt et al., 2015, Puri et al., 2009). Zelber-Sagi et al. also reported that lower total fat intake and a higher intake of fish oils, such as docosahexaenoic acid (DHA), may be beneficial for treating NASH (Zelber-Sagi et al., 2007). G-protein coupled receptor 120/free fatty acid receptor 4 (GPR120/FFAR4) is the functional receptor for n−3 PUFAs and is expressed in the adipose tissue (Gotoh et al., 2007), intestinal tract (Hirasawa et al., 2005), macrophages (Oh et al., 2010) and Kupffer cells (Raptis et al., 2014). These receptor ligands have been shown to elicit anti-inflammatory and insulin sensitizing effects (Hirasawa et al., 2005, Oh et al., 2010, Oh et al., 2014, Ichimura et al., 2012, Raptis et al., 2014) in mice models as well as in clinical studies (Ichimura et al., 2012, Marzuillo et al., 2014, Nobili et al., 2014). Indeed, DHA inhibits the nuclear factor kappa B (NF-κB) and Jun-N-terminal kinase pathways, and attenuates the inflammatory response via GPR120/FFAR4 (Oh et al., 2010, Raptis et al., 2014). Furthermore, human genetic variants in the GPR120/FFAR4 gene predispose to obesity and diabetes (Ichimura et al., 2012, Waguri et al., 2013, Marzuillo et al., 2014). Recent studies showed that a nonsynonymous variant (p.R270H) of GPR120/FFAR4 in pediatric NAFLD patients was associated with increased alanine transaminase (ALT) levels (Marzuillo et al., 2014, Nobili et al., 2014). The p.R270H variant is considered to enhance inflammation in adipose and hepatic tissues, which suggests an important role of this receptor in the development of NASH et al., 2014; Nobili et al., 2014)).