Exhaustive Training Leads to Hepatic Fat Accumulation

Rocha, Aristides Almeida; Pinto, Ana P.; Teixeira, Giovana Rampazzo; Pereira, Bruno; Oliveira, Luciana Coutinho de; Silva, Adriana C.; Morais, Gustavo P.; Cintra, Dennys Esper; Pauli, José Rodrigo; Silva, Adelino Sánchez Ramos da

doi:10.1002/jcp.25625

Cited by 17 publications

(21 citation statements)

References 49 publications

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“…The slices were stained with hematoxylin for 10 min or with oil red O solution (Sigma-Aldrich) for 25 min, washed and stained with eosin (5 min). The slices stained with oil red O were used to analyses of lipid droplets area and red stained area using ImageJ (Schneider et al 2012) program using the 40× image, in agreement with previous studies (Botezelli et al 2016, da Rocha et al 2017, Muñoz et al 2018).…”

Section: Liver Hematoxylin-eosin Histology and Oil Red O Stainingmentioning

confidence: 78%

Short-term strength training reduces gluconeogenesis and NAFLD in obese mice

Pereira

Rodrigues

Anaruma

et al. 2019

Journal of Endocrinology

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Non-alcoholic fatty liver disease (NAFLD) has a positive correlation with obesity, insulin resistance and type 2 diabetes mellitus (T2D). The aerobic training is an important tool in combating NAFLD. However, no studies have demonstrated the molecular effects of short-term strength training on the accumulation of hepatic fat in obese mice. This study aimed to investigate the effects of short-term strength training on the mechanisms of oxidation and lipid synthesis in the liver of obese mice. The short duration protocol was used to avoid changing the amount of adipose tissue. Swiss mice were separated into three groups: lean control (CTL), sedentary obese (OB) and strength training obese (STO). The obese groups were fed a high-fat diet (HFD) and the STO group performed the strength training protocol 1 session/day for 15 days. The short-term strength training reduced hepatic fat accumulation, increasing hepatic insulin sensitivity and controlling hepatic glucose production. The obese animals increased the mRNA of lipogenic genes Fasn and Scd1 and reduced the oxidative genes Cpt1a and Ppara. On the other hand, the STO group presented the opposite results. Finally, the obese animals presented higher levels of lipogenic proteins (ACC and FAS) and proinflammatory cytokines (TNF-α and IL-1β), but the short-term strength training was efficient in reducing this condition, regardless of body weight loss. In conclusion, there was a reduction of obesity-related hepatic lipogenesis and inflammation after short-term strength training, independent of weight loss, leading to improvements in hepatic insulin sensitivity and glycemic homeostasis in obese mice. Key points: (1) Short-term strength training (STST) reduced fat accumulation and inflammation in the liver; (2) Hepatic insulin sensitivity and HPG control were increased with STST; (3) The content and activity of ACC and content of FAS were reduced with STST; (4) STST improved hepatic fat accumulation and glycemic homeostasis; (5) STST effects were observed independently of body weight change.

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Section: Liver Hematoxylin-eosin Histology and Oil Red O Stainingmentioning

confidence: 78%

Short-term strength training reduces gluconeogenesis and NAFLD in obese mice

Pereira

Rodrigues

Anaruma

et al. 2019

Journal of Endocrinology

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“…Recently, our research group showed that mice subjected to a downhill running–based overtraining (OTR/down) protocol presented elevated levels of proinflammatory cytokines in the serum, hypothalamus, muscle, and liver (da Rocha, Pinto, et al, ; Pereira et al, ). Also, this OTR/down model induces the nonfunctional overreaching (NFOR) state (da Rocha et al, , ), which is defined as a performance decrement or stagnation that may be reversed after weeks/months of recovery (Meeusen et al, ).…”

Section: Introductionmentioning

confidence: 99%

Excessive training induces molecular signs of pathologic cardiac hypertrophy

Rocha

Teixeira

Pinto

et al. 2018

Journal Cellular Physiology

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Chronic exercise induces cardiac remodeling that promotes left ventricular hypertrophy and cardiac functional improvement, which are mediated by the mammalian or the mechanistic target of rapamycin (mTOR) as well as by the androgen and glucocorticoid receptors (GRs). However, pathological conditions (i.e., chronic heart failure, hypertension, and aortic stenosis, etc.) also induce cardiac hypertrophy, but with detrimental function, high levels of proinflammatory cytokines and myostatin, elevated fibrosis, reduced adenosine monophosphate-activated protein kinase (AMPK) activation, and fetal gene reactivation. Furthermore, recent studies have evidenced that excessive training induced an inflammatory status in the serum, muscle, hypothalamus, and liver, suggesting a pathological condition that could also be detrimental to cardiac tissue. Here, we verified the effects of three running overtraining (OT) models on the molecular parameters related to physiological and pathological cardiac hypertrophy. C57BL/6 mice performed three different OT protocols and were evaluated for molecular parameters related to physiological and pathological cardiac hypertrophy, including immunoblotting, reverse transcription polymerase chain reaction, histology, and immunohistochemistry analyses. In summary, the three OT protocols induced left ventricle (LV) hypertrophy with signs of cardiac fibrosis and negative morphological adaptations. These maladaptations were accompanied by reductions in AMPKalpha (Thr172) phosphorylation, androgen receptor, and GR expressions, as well as by an increase in interleukin-6 expression. Specifically, the downhill running-based OT model reduced the content of some proteins related to the mTOR signaling pathway and upregulated the β-isoform of myosin heavy-chain gene expression, presenting signs of LV pathological hypertrophy development.

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“…As soon as anesthesia was confirmed by the loss of the pedal reflexes, the abdominal cavity was opened, the portal vein was exposed, and saline with and without human recombinant insulin (10 U.kg -1 , Eli Lilly, Indianapolis, IN) was injected. At 90 s after saline or saline with human recombinant insulin injection (Pauli et al 2008, Ropelle et al 2006, gastrocnemius samples were removed and used for immunoblotting analysis as previously described (da Rocha et al 2015, da Rocha et al 2016a, da Rocha et al 2017, Pereira et al 2015a, Pereira et al 2015b, Pereira et al 2014a, Pereira et al 2014b. Herein, we used the following antibodies: beta-actin (SC69879), GLUT-4 (SC53566) and PGC-1α (SC13067) from Santa Cruz Biotechnology (Santa Cruz, CA, USA) at dilution of 1:750; Akt (CELL9272S), phospho-Akt (Ser473; CELL4058S), AMPKα (CELL2532S), phospho(p)-AMPKα (Thr172; CELL2535S) and GLUT-1 (CELL12939S) from Cell Signaling Technology (Beverly, MA, USA) at dilution of 1:1,000.…”

Section: Methodsmentioning

confidence: 99%

Uphill Running Excessive Training Increases Gastrocnemius Glycogen Content in C57BL/6 Mice

Morais

Rocha²,

Pinto³

et al. 2018

Physiol Res

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The main aim of the present investigation was to verify the effects of three overtraining (OT) protocols performed in downhill (OTR/down), uphill (OTR/up) and without inclination (OTR) on the protein levels of Akt (Ser473), AMPKα (Thr172), PGC-1α, plasma membrane GLUT-1 and GLUT-4 as well as on the glycogen contents in mice gastrocnemius. A trained (TR) protocol was used as positive control. Rodents were divided into naïve (N, sedentary mice), control (CT, sedentary mice submitted to the performance evaluations), TR, OTR/down, OTR/up and OTR groups. At the end of the experimental protocols, gastrocnemius samples were removed and used for immunoblotting analysis as well as for glycogen measurements. There was no significant difference between the experimental groups for the protein levels of pAkt (Ser473), pAMPKα (Thr172), PGC-1α, plasma membrane GLUT-1 and GLUT-4. However, the OTR/up protocol exhibited higher contents of glycogen compared to the CT and TR groups. In summary, the OTR/up group increased the gastrocnemius glycogen content without significant changes of pAkt (Ser473), pAMPKα (Thr172), PGC-1α, plasma membrane GLUT-1 and GLUT-4.

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Exhaustive Training Leads to Hepatic Fat Accumulation

Cited by 17 publications

References 49 publications

Short-term strength training reduces gluconeogenesis and NAFLD in obese mice

Short-term strength training reduces gluconeogenesis and NAFLD in obese mice

Excessive training induces molecular signs of pathologic cardiac hypertrophy

Uphill Running Excessive Training Increases Gastrocnemius Glycogen Content in C57BL/6 Mice

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