Improved Insulin Sensitivity After Exercise: Focus on Insulin Signaling
After a single bout of exercise, the ability of insulin to stimulate glucose uptake is markedly improved locally in the previously active muscles. This makes exercise a potent stimulus counteracting insulin resistance characterizing type 2 diabetes (T2D). It is believed that at least part of the mec...
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Published in | Obesity (Silver Spring, Md.) Vol. 17; no. n3s; pp. S15 - S20 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.12.2009
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Abstract | After a single bout of exercise, the ability of insulin to stimulate glucose uptake is markedly improved locally in the previously active muscles. This makes exercise a potent stimulus counteracting insulin resistance characterizing type 2 diabetes (T2D). It is believed that at least part of the mechanism relates to an improved ability of insulin to stimulate translocation of glucose transporters (GLUT4) to the muscle membrane after exercise. How this is accomplished is still unclear; however, an obvious possibility is that exercise interacts with the insulin signaling pathway to GLUT4 translocation allowing for a more potent insulin response. Parallel to unraveling of the insulin signaling cascade, this has been investigated within the past 25 years. Reviewing existing studies clearly indicates that improved insulin action can occur independent of interactions with proximal insulin signaling. In contrast, more recent observations indicate that interactions exist at the distal signaling level of AS160 and atypical protein kinase C (aPKC). Although the functional interpretation is lacking, these novel observations may present a breakthrough in understanding the beneficial interplay between exercise and insulin action. |
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AbstractList | After a single bout of exercise, the ability of insulin to stimulate glucose uptake is markedly improved locally in the previously active muscles. This makes exercise a potent stimulus counteracting insulin resistance characterizing type 2 diabetes (T2D). It is believed that at least part of the mechanism relates to an improved ability of insulin to stimulate translocation of glucose transporters (GLUT4) to the muscle membrane after exercise. How this is accomplished is still unclear; however, an obvious possibility is that exercise interacts with the insulin signaling pathway to GLUT4 translocation allowing for a more potent insulin response. Parallel to unraveling of the insulin signaling cascade, this has been investigated within the past 25 years. Reviewing existing studies clearly indicates that improved insulin action can occur independent of interactions with proximal insulin signaling. In contrast, more recent observations indicate that interactions exist at the distal signaling level of AS160 and atypical protein kinase C (aPKC). Although the functional interpretation is lacking, these novel observations may present a breakthrough in understanding the beneficial interplay between exercise and insulin action. |
Author | Richter, Erik A Frosig, Christian |
Author_xml | – sequence: 1 fullname: Frosig, Christian – sequence: 2 fullname: Richter, Erik A |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19927140$$D View this record in MEDLINE/PubMed |
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Snippet | After a single bout of exercise, the ability of insulin to stimulate glucose uptake is markedly improved locally in the previously active muscles. This makes... |
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SubjectTerms | Biological Transport Blood Glucose - metabolism Diabetes Exercise Exercise - physiology Glucose Glucose Transporter Type 4 - metabolism glucose transporters Homeostasis Humans insulin Insulin - metabolism Insulin resistance Insulin Resistance - physiology Kinases Muscle, Skeletal - metabolism muscles Musculoskeletal system noninsulin-dependent diabetes mellitus obesity Phosphorylation Physical fitness Physiology protein kinase C Proteins signal transduction Signal Transduction - physiology |
Title | Improved Insulin Sensitivity After Exercise: Focus on Insulin Signaling |
URI | http://dx.doi.org/10.1038/oby.2009.383 https://onlinelibrary.wiley.com/doi/abs/10.1038%2Foby.2009.383 https://www.ncbi.nlm.nih.gov/pubmed/19927140 https://www.proquest.com/docview/1030381144 https://search.proquest.com/docview/734256401 |
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