Improved insulin sensitivity after exercise: focus on insulin signaling

Publikation: Bidrag til tidsskriftReviewForskning

Standard

Improved insulin sensitivity after exercise: focus on insulin signaling. / Frøsig, Christian; Richter, Erik A.

I: Obesity, Bind 17, Nr. Suppl. 3, 2009, s. S15-S20.

Publikation: Bidrag til tidsskriftReviewForskning

Harvard

Frøsig, C & Richter, EA 2009, 'Improved insulin sensitivity after exercise: focus on insulin signaling', Obesity, bind 17, nr. Suppl. 3, s. S15-S20. https://doi.org/10.1038/oby.2009.383

APA

Frøsig, C., & Richter, E. A. (2009). Improved insulin sensitivity after exercise: focus on insulin signaling. Obesity, 17(Suppl. 3), S15-S20. https://doi.org/10.1038/oby.2009.383

Vancouver

Frøsig C, Richter EA. Improved insulin sensitivity after exercise: focus on insulin signaling. Obesity. 2009;17(Suppl. 3):S15-S20. https://doi.org/10.1038/oby.2009.383

Author

Frøsig, Christian ; Richter, Erik A. / Improved insulin sensitivity after exercise: focus on insulin signaling. I: Obesity. 2009 ; Bind 17, Nr. Suppl. 3. s. S15-S20.

Bibtex

@article{2acb477052ce11df928f000ea68e967b,
title = "Improved insulin sensitivity after exercise: focus on insulin signaling",
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.",
author = "Christian Fr{\o}sig and Richter, {Erik A.}",
note = "Keywords: Biological Transport; Blood Glucose; Exercise; Glucose Transporter Type 4; Humans; Insulin; Insulin Resistance; Muscle, Skeletal; Signal Transduction",
year = "2009",
doi = "10.1038/oby.2009.383",
language = "English",
volume = "17",
pages = "S15--S20",
journal = "Obesity",
issn = "1930-7381",
publisher = "Wiley-Blackwell",
number = "Suppl. 3",

}

RIS

TY - JOUR

T1 - Improved insulin sensitivity after exercise: focus on insulin signaling

AU - Frøsig, Christian

AU - Richter, Erik A.

N1 - Keywords: Biological Transport; Blood Glucose; Exercise; Glucose Transporter Type 4; Humans; Insulin; Insulin Resistance; Muscle, Skeletal; Signal Transduction

PY - 2009

Y1 - 2009

N2 - 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.

AB - 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.

U2 - 10.1038/oby.2009.383

DO - 10.1038/oby.2009.383

M3 - Review

C2 - 19927140

VL - 17

SP - S15-S20

JO - Obesity

JF - Obesity

SN - 1930-7381

IS - Suppl. 3

ER -

ID: 19437201