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      Lean and Obese Zucker Rat Extensor Digitorum Longus Muscle high-frequency electrical stimulation (HFES) Data: Regulation of p70S6kinase Associated Proteins

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          Abstract

          Anaerobic exercise has been advocated as a prescribed treatment for the management of diabetes: however, alterations in exercise-induced signaling remain largely unexplored in the diabetic muscle. Here, we compare the basal and the in situ contraction-induced phosphorylation of the AKT, GSK3beta, mTor, p70s6K, Pten, and Shp2 in the lean and obese (fa/fa) Zucker rat Extensor Digitorum Longus (EDL) muscle following a single bout of contractile stimuli. This article represents data associated with prior publications from our lab (Katta et al., 2009a, 2009b; Tullgren et al., 1991) [1– 3] and concurrent Data in Brief articles (Ginjupalli et al., 2017a, 2017b; Rice et al., 2017a, 2017b) [4– 7].

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          Phosphorylation of p70(S6k) correlates with increased skeletal muscle mass following resistance exercise.

          K Baar, K Esser (1998)
          High-resistance exercise training results in an increase in muscle wet mass and protein content. To begin to address the acute changes following a single bout of high-resistance exercise, a new model has been developed. Training rats twice a week for 6 wk resulted in 13.9 and 14.4% hypertrophy in the extensor digitorum longus (EDL) and tibialis anterior (TA) muscles, respectively. Polysome profiles after high-resistance lengthening contractions suggest that the rate of initiation is increased. The activity of the 70-kDa S6 protein kinase (p70(S6k)), a regulator of translation initiation, is also increased following high-resistance lengthening contractions (TA, 363 +/- 29%; EDL, 353 +/- 39%). Furthermore, the increase in p70(S6k) activity 6 h after exercise correlates with the percent change in muscle mass after 6 wk of training (r = 0.998). The tight correlation between the activation of p70(S6k) and the long-term increase in muscle mass suggests that p70(S6k) phosphorylation may be a good marker for the phenotypic changes that characterize muscle hypertrophy and may play a role in load-induced skeletal muscle growth.
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            Altered Regulation of Contraction-Induced Akt/mTOR/p70S6k Pathway Signaling in Skeletal Muscle of the Obese Zucker Rat

            Anjaiah Katta, Sunil Kakarla, Miaozong Wu … (2009)
            Increased muscle loading results in the phosphorylation of the 70 kDa ribosomal S6 kinase (p70S6k), and this event is strongly correlated with the degree of muscle adaptation following resistance exercise. Whether insulin resistance or the comorbidities associated with this disorder may affect the ability of skeletal muscle to activate p70S6k signaling following an exercise stimulus remains unclear. Here, we compare the contraction-induced activation of p70S6k signaling in the plantaris muscles of lean and insulin resistant obese Zucker rats following a single bout of increased contractile loading. Compared to lean animals, the basal phosphorylation of p70S6k (Thr389; 37.2% and Thr421/Ser424; 101.4%), Akt (Thr308; 25.1%), and mTOR (Ser2448; 63.0%) was higher in obese animals. Contraction increased the phosphorylation of p70S6k (Thr389), Akt (Ser473), and mTOR (Ser2448) in both models however the magnitude and kinetics of activation differed between models. These results suggest that contraction-induced activation of p70S6k signaling is altered in the muscle of the insulin resistant obese Zucker rat.
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              Lean and obese Zucker rats exhibit different patterns of p70s6 kinase regulation in the tibialis anterior muscle in response to high-force muscle contraction.

              Anjaiah Katta, S. Karkala, Eric Blough … (2009)
              Increased phosphorylation of the 70-kDa ribosomal S6 kinase (p70S6k) signaling is strongly correlated with the degree of muscle adaptation following exercise. Herein we compare the phosphorylation of p70S6k, Akt, and mammalian target of rapamycin (mTOR) in the tibialis anterior (TA) muscles of lean and obese Zucker rats following a bout of eccentric exercise. Exercise increased p70S6k (Thr389) phosphorylation immediately after (33.3+/-7.2%) and during [1 h (24.0+/-14.9%) and 3 h (24.6+/-11.3%)] recovery in the lean TA and at 3 h (33.5+/-8.0%) in the obese TA Zucker rats. mTOR (Ser2448) phosphorylation was elevated in the lean TA immediately after exercise (96.5+/-40.3%) but remained unaltered in the obese TA. Exercise increased Akt (Thr308) and Akt (Ser473) phosphorylation in the lean but not the obese TA. These results suggest that insulin resistance is associated with alterations in the ability of muscle to activate p70S6k signaling following an acute bout of exercise.
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                Author and article information

                Contributors
                Kevin M. Rice
                Journal
                Journal ID (nlm-ta): Data Brief
                Journal ID (iso-abbrev): Data Brief
                Title: Data in Brief
                Publisher: Elsevier
                ISSN (Electronic): 2352-3409
                Publication date PMC-release: 20 November 2017
                Publication date Collection: February 2018
                Publication date (Electronic): 20 November 2017
                Volume: 16
                Pages: 430-441
                Affiliations
                [a ]Center for Diagnostic Nanosystems, Marshall University, Huntington, WV, USA
                [b ]Department of Internal Medicine, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, USA
                [c ]Biotechnology Graduate Program West Virginia State University, Institute, WV, USA
                [d ]Department of Health and Human Service, School of Kinesiology, Marshall University, Huntington, WV, USA
                [e ]Department of Public Heath, Marshall University, Huntington, WV, USA
                [f ]College of Health, Science, and Technology, University of Central Missouri, Warrensburg, MO, USA
                [g ]School of Education, Health, and Human Performance, Fairmont State University, Fairmont, WV, USA
                [h ]Department of Pharmaceutical Sciences and Research, School of Pharmacy, Marshall University, Huntington, WV, USA
                [i ]Department of Pharmacology, Physiology and Toxicology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, USA
                Author notes
                [* ]Correspondence to: Center for Diagnostic Nanosystems, Robert C. Byrd Biotechnology Science Center, Marshall University, Room 241D, 1700 3rd Ave., Huntington, WV 25755-1090, USA. Fax: +304 696 3766.Center for Diagnostic Nanosystems, Robert C. Byrd Biotechnology Science Center, Marshall UniversityRoom 241D, 1700 3rd AveHuntingtonWV25755-1090USA rice9@ 123456marshall.edu
                Article
                Publisher ID: S2352-3409(17)30647-9
                DOI: 10.1016/j.dib.2017.11.051
                PMC ID: 5723369
                SO-VID: a0f91ad7-45e6-49bd-9dc4-554d2df7db3a
                Copyright © © 2017 The Authors
                License:

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 15 September 2017
                Date revision received : 13 November 2017
                Date accepted : 15 November 2017
                Categories
                Subject: Genetics, Genomics and Molecular Biology

                Keywords: diabetes,skeletal muscle,high-frequency electrical stimulation (hfes),zucker rat,extensor digitorum longus,p70s6k
                Data availability:
                Keywords: diabetes, skeletal muscle, high-frequency electrical stimulation (hfes), zucker rat, extensor digitorum longus, p70s6k

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