45
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Frequent interruptions of sedentary time modulates contraction- and insulin-stimulated glucose uptake pathways in muscle: Ancillary analysis from randomized clinical trials

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Epidemiological studies have observed associations between frequent interruptions of sitting time with physical activity bouts and beneficial metabolic outcomes, even in individuals who regularly exercise. Frequent interruptions to prolonged sitting reduce postprandial plasma glucose. Here we studied potential skeletal muscle mechanisms accounting for this improved control of glycemia in overweight adults under conditions of one day uninterrupted sitting and sitting interrupted with light-intensity or moderate-intensity walking every 20-min (n = 8); and, after three days of either uninterrupted sitting or light-intensity walking interruptions (n = 5). Contraction- and insulin-mediated glucose uptake signaling pathways as well as changes in oxidative phosphorylation proteins were examined. We showed that 1) both interventions reduce postprandial glucose concentration, 2) acute interruptions to sitting over one day stimulate the contraction-mediated glucose uptake pathway, 3) both acute interruptions to sitting with moderate-intensity activity over one day and light-intensity activity over three days induce a transition to modulation of the insulin-signaling pathway, in association with increased capacity for glucose transport. Only the moderate-intensity interruptions resulted in greater capacity for glycogen synthesis and likely for ATP production. These observations contribute to a mechanistic explanation of improved postprandial glucose metabolism with regular interruptions to sitting time, a promising preventive strategy for metabolic diseases.

          Related collections

          Most cited references50

          • Record: found
          • Abstract: found
          • Article: not found

          Inhibition of glycogen synthase kinase-3 by insulin mediated by protein kinase B.

          Glycogen synthase kinase-3 (GSK3) is implicated in the regulation of several physiological processes, including the control of glycogen and protein synthesis by insulin, modulation of the transcription factors AP-1 and CREB, the specification of cell fate in Drosophila and dorsoventral patterning in Xenopus embryos. GSK3 is inhibited by serine phosphorylation in response to insulin or growth factors and in vitro by either MAP kinase-activated protein (MAPKAP) kinase-1 (also known as p90rsk) or p70 ribosomal S6 kinase (p70S6k). Here we show, however, that agents which prevent the activation of both MAPKAP kinase-1 and p70S6k by insulin in vivo do not block the phosphorylation and inhibition of GSK3. Another insulin-stimulated protein kinase inactivates GSK3 under these conditions, and we demonstrate that it is the product of the proto-oncogene protein kinase B (PKB, also known as Akt/RAC). Like the inhibition of GSK3 (refs 10, 14), the activation of PKB is prevented by inhibitors of phosphatidylinositol (PI) 3-kinase.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Breaks in sedentary time: beneficial associations with metabolic risk.

            Total sedentary (absence of whole-body movement) time is associated with obesity, abnormal glucose metabolism, and the metabolic syndrome. In addition to the effects of total sedentary time, the manner in which it is accumulated may also be important. We examined the association of breaks in objectively measured sedentary time with biological markers of metabolic risk. Participants (n = 168, mean age 53.4 years) for this cross-sectional study were recruited from the 2004-2005 Australian Diabetes, Obesity and Lifestyle study. Sedentary time was measured by an accelerometer (counts/minute(-1) or = 100) was considered a break. Fasting plasma glucose, 2-h plasma glucose, serum triglycerides, HDL cholesterol, weight, height, waist circumference, and resting blood pressure were measured. MatLab was used to derive the breaks variable; SPSS was used for the statistical analysis. Independent of total sedentary time and moderate-to-vigorous intensity activity time, increased breaks in sedentary time were beneficially associated with waist circumference (standardized beta = -0.16, 95% CI -0.31 to -0.02, P = 0.026), BMI (beta = -0.19, -0.35 to -0.02, P = 0.026), triglycerides (beta = -0.18, -0.34 to -0.02, P = 0.029), and 2-h plasma glucose (beta = -0.18, -0.34 to -0.02, P = 0.025). This study provides evidence of the importance of avoiding prolonged uninterrupted periods of sedentary (primarily sitting) time. These findings suggest new public health recommendations regarding breaking up sedentary time that are complementary to those for physical activity.
              Bookmark
              • Record: found
              • Abstract: not found
              • Article: not found

              The effect of insulin on the disposal of intravenous glucose. Results from indirect calorimetry and hepatic and femoral venous catheterization.

                Bookmark

                Author and article information

                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group
                2045-2322
                24 August 2016
                2016
                : 6
                : 32044
                Affiliations
                [1 ]Physical Activity Laboratory, Baker IDI Heart and Diabetes Institute , Melbourne, Victoria 3004, Australia
                [2 ]Anschutz Health and Wellness Center, Division of Endocrinology, Metabolism and Diabetes, University of Colorado , Aurora, Colorado 80045, USA
                [3 ]Metabolic and Vascular Physiology Laboratory, Baker IDI Heart and Diabetes Institute , Melbourne, Victoria 3004, Australia
                [4 ]Department of Medicine, Monash University , Melbourne, Victoria 3800, Australia
                [5 ]Behavioral Epidemiology Laboratory, Baker IDI Heart and Diabetes Institute , Melbourne, Victoria 3004, Australia
                [6 ]Melbourne School of Population Health, The University of Melbourne , Melbourne, Victoria 3010, Australia
                [7 ]School of Public Health, the University of Queensland , St Lucia, Queensland 4072, Australia
                [8 ]School of Exercise and Nutrition Sciences, Deakin University , Burwood, Victoria 3125, Australia
                [9 ]Department of Epidemiology and Preventive Medicine, Monash University , Melbourne, Victoria 3800, Australia
                [10 ]Mary MacKillop Institute for Health Research, Australian Catholic University , Melbourne, Victoria 3000, Australia
                [11 ]School of Sport Science, Exercise and Health, The University Of Western Australia , 35 Stirling Hwy, Crawley, Perth, Western Australia
                [12 ]Department of Physiology, Monash University , Melbourne, Victoria 3800, Australia
                [13 ]Department of Physiology, The University of Melbourne , Parkville, Victoria 3010, Australia
                Author notes
                Article
                srep32044
                10.1038/srep32044
                4995429
                27554943
                41439ceb-8597-4606-ad00-d518c634163b
                Copyright © 2016, The Author(s)

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                : 11 February 2016
                : 27 July 2016
                Categories
                Article

                Uncategorized
                Uncategorized

                Comments

                Comment on this article