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Retracted

Mediators of Inflammation has retracted this article. After a concern was raised to them by a reader, the authors contacted the journal to replace the anti-ACC blot in Figure (b), providing the original figure. The journal found that the published blot in Figure (b) was similar in other articles [29]. Due to this, the journal reassessed the other figures and found that, for the β-actin bands in Figure (c), lanes 3 and 4 are similar to lanes 5 and 6, respectively. Although the authors provided the journal with the underlying blots for all the figures, the journal and authors decided to retract the manuscript. The replacement blot for Figure (b) and the underlying blots for all figures are available in the Supplementary Materials. The authors stated that the representative loading control bands in Figures (c) and (b) were improperly assembled, leading to repetitions of bands, and that these errors do not affect the results, once several papers have demonstrated that exercise does not change both, ACC [10, 11] and actin [1214] protein content, in the skeletal muscle of rodents. In light of the figure preparation issues, the authors sincerely apologize to the scientific community for any misunderstanding that these errors may have caused.

View the full Retraction here.

References

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  2. L. S. S. Pauli, E. C. C. Ropelle, C. T. de Souza et al., “Exercise training decreases mitogen-activated protein kinase phosphatase-3 expression and suppresses hepatic gluconeogenesis in obese mice,” Journal of Physiology, vol. 592, no. 6, pp. 1325–1340, 2014.
  3. E. C. Chiarreotto-Ropelle, L. S. S. Pauli, C. K. Katashima et al., “Acute exercise suppresses hypothalamic PTP1B protein level and improves insulin and leptin signaling in obese rats,” American Journal of Physiology - Endocrinology and Metabolism, vol. 305, no. 5, pp. E649–E659, 2013.
  4. E. R. Ropelle, M. B. Flores, D. E. Cintra, G. Z. Rocha, Pauli. J. r et al., “IL-6 and IL-10 Anti-Inflammatory Activity Links Exercise to Hypothalamic Insulin and Leptin Sensitivity through IKKβ and ER Stress Inhibition,” PLOS Biology, vol. 8, no. 8, Article ID e1000465, 2010.
  5. Flores, B. S. Marcelo et al., “Obesity-Induced Increase in Tumor Necrosis Factor-α Leads to Development of Colon Cancer in Mice,” Gastroenterology, vol. 143, no. 3, pp. 741–753.e4, 2012, http://dx.doi.org/10.1053/j.gastro.2012.05.045.
  6. P. O. Prada, P. G. F. Quaresma, A. M. Caricilli et al., “Tub has a key role in insulin and leptin signaling and action in vivo in hypothalamic nuclei,” Diabetes, vol. 62, no. 1, pp. 137–148, 2013.
  7. V. A. Barbosa, T. F. Luciano, S. O. Marques et al., “Acute exercise induce endothelial nitric oxide synthase phosphorylation via Akt and AMP-activated protein kinase in aorta of rats: Role of reactive oxygen species,” International Journal of Cardiology, vol. 167, no. 6, pp. 2983–2988, 2013.
  8. Statement of Retraction, “Tub Has a Key Role in Insulin and Leptin Signaling and Action In Vivo in Hypothalamic Nuclei,” Diabetes, vol. 62, pp. 137–148, 2013.
  9. J. Expression of concern. Physiol, “Expression of concern,” The Journal of Physiology, vol. 594, pp. 5027-5028, 2016.
  10. H. M. O’Neill, J. S. Lally, S. Galic et al., “Skeletal muscle ACC2 S212 phosphorylation is not required for the control of fatty acid oxidation during exercise,” Physiological Reports, vol. 3, no. 7, Article ID e12444, 2015.
  11. R. A. Gulli, J. M. Tishinsky, T. MacDonald, L. E. Robinson, D. C. Wright, and D. J. Dyck, “Exercise restores insulin, but not adiponectin, response in skeletal muscle of high-fat fed rodents,” American Journal of Physiology - Regulatory Integrative and Comparative Physiology, vol. 303, no. 10, pp. R1062–R1070, 2012.
  12. C. He, M. C. Bassik, V. Moresi et al., “Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis,” Nature, vol. 481, no. 7382, pp. 511–515, 2012.
  13. J. H. Woo, K. O. Shin, Y. H. Lee, K. S. Jang, J. Y. Bae, and H. T. Roh, “Effects of treadmill exercise on skeletal muscle mTOR signaling pathway in high-fat diet-induced obese mice,” Journal of Physical Therapy Science, vol. 28, no. 4, pp. 1260–1265, 2016.
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Mediators of Inflammation
Volume 2014, Article ID 987017, 11 pages
http://dx.doi.org/10.1155/2014/987017
Research Article

Treadmill Training Increases SIRT-1 and PGC-1α Protein Levels and AMPK Phosphorylation in Quadriceps of Middle-Aged Rats in an Intensity-Dependent Manner

1Laboratory of Exercise Biochemistry and Physiology, Health Sciences Unit, Extremo Sul Catarinense University (UNESC), 88806-000 Criciuma, SC, Brazil
2Faculty of Applied Sciences, University of Campinas (UNICAMP), 13083-872 Limeira, SP, Brazil
3Post Graduation Program in Motricity Science, Instituto de Biociências, São Paulo State University (UNESP), 13506-900 Rio Claro, SP, Brazil
4Human Movement Laboratory, São Judas Tadeu University, 03166-000 São Paulo, SP, Brazil
5Immunometabolism Research Group, Department of Physical Education, São Paulo State University (UNESP), 19060-900 Presidente Prudente, SP, Brazil
6School of Physical Education and Sport of Ribeirão Preto, São Paulo University (USP), 14040-907 Ribeirão Preto, SP, Brazil

Received 19 February 2014; Revised 8 April 2014; Accepted 15 April 2014; Published 9 June 2014

Academic Editor: José Cesar Rosa

Copyright © 2014 Nara R. C. Oliveira et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The present study investigated the effects of running at 0.8 or 1.2 km/h on inflammatory proteins (i.e., protein levels of TNF-α, IL-1β, and NF-κB) and metabolic proteins (i.e., protein levels of SIRT-1 and PGC-1α, and AMPK phosphorylation) in quadriceps of rats. Male Wistar rats at 3 (young) and 18 months (middle-aged rats) of age were divided into nonexercised (NE) and exercised at 0.8 or 1.2 km/h. The rats were trained on treadmill, 50 min per day, 5 days per week, during 8 weeks. Forty-eight hours after the last training session, muscles were removed, homogenized, and analyzed using biochemical and western blot techniques. Our results showed that: (a) running at 0.8 km/h decreased the inflammatory proteins and increased the metabolic proteins compared with NE rats; (b) these responses were lower for the inflammatory proteins and higher for the metabolic proteins in young rats compared with middle-aged rats; (c) running at 1.2 km/h decreased the inflammatory proteins and increased the metabolic proteins compared with 0.8 km/h; (d) these responses were similar between young and middle-aged rats when trained at 1.2 km. In summary, the age-related increases in inflammatory proteins, and the age-related declines in metabolic proteins can be reversed and largely improved by treadmill training.