Role of AMP-activated protein kinase for regulating post-exercise insulin sensitivity
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Role of AMP-activated protein kinase for regulating post-exercise insulin sensitivity. / Kjøbsted, Rasmus; Wojtaszewski, Jørgen; Treebak, Jonas Thue.
AMP-activated Protein Kinase. ed. / M D Cordero; B Viollet. Springer, 2016. p. 81-126 (E X S, Vol. 107).Research output: Chapter in Book/Report/Conference proceeding › Book chapter › Research › peer-review
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TY - CHAP
T1 - Role of AMP-activated protein kinase for regulating post-exercise insulin sensitivity
AU - Kjøbsted, Rasmus
AU - Wojtaszewski, Jørgen
AU - Treebak, Jonas Thue
N1 - CURIS 2016 NEXS 324
PY - 2016
Y1 - 2016
N2 - Skeletal muscle insulin resistance precedes development of type 2 diabetes (T2D). As skeletal muscle is a major sink for glucose disposal, understanding the molecular mechanisms involved in maintaining insulin sensitivity of this tissue could potentially benefit millions of people that are diagnosed with insulin resistance. Regular physical activity in both healthy and insulin-resistant individuals is recognized as the single most effective intervention to increase whole-body insulin sensitivity and thereby positively affect glucose homeostasis. A single bout of exercise has long been known to increase glucose disposal in skeletal muscle in response to physiological insulin concentrations. While this effect is identified to be restricted to the previously exercised muscle, the molecular basis for an apparent convergence between exercise- and insulin-induced signaling pathways is incompletely known. In recent years, we and others have identified the Rab GTPase-activating protein, TBC1 domain family member 4 (TBC1D4) as a target of key protein kinases in the insulin- and exercise-activated signaling pathways. Our working hypothesis is that the AMP-activated protein kinase (AMPK) is important for the ability of exercise to insulin sensitize skeletal muscle through TBC1D4. Here, we aim to provide an overview of the current available evidence linking AMPK to post-exercise insulin sensitivity.
AB - Skeletal muscle insulin resistance precedes development of type 2 diabetes (T2D). As skeletal muscle is a major sink for glucose disposal, understanding the molecular mechanisms involved in maintaining insulin sensitivity of this tissue could potentially benefit millions of people that are diagnosed with insulin resistance. Regular physical activity in both healthy and insulin-resistant individuals is recognized as the single most effective intervention to increase whole-body insulin sensitivity and thereby positively affect glucose homeostasis. A single bout of exercise has long been known to increase glucose disposal in skeletal muscle in response to physiological insulin concentrations. While this effect is identified to be restricted to the previously exercised muscle, the molecular basis for an apparent convergence between exercise- and insulin-induced signaling pathways is incompletely known. In recent years, we and others have identified the Rab GTPase-activating protein, TBC1 domain family member 4 (TBC1D4) as a target of key protein kinases in the insulin- and exercise-activated signaling pathways. Our working hypothesis is that the AMP-activated protein kinase (AMPK) is important for the ability of exercise to insulin sensitize skeletal muscle through TBC1D4. Here, we aim to provide an overview of the current available evidence linking AMPK to post-exercise insulin sensitivity.
KW - Faculty of Science
KW - AMP-activated protein kinase
KW - Exercise
KW - Skeletal muscle
KW - Glucose uptake
KW - TBC1D4
KW - AS160
KW - Insulin sensitivity
U2 - 10.1007/978-3-319-43589-3_5
DO - 10.1007/978-3-319-43589-3_5
M3 - Book chapter
C2 - 27812978
SN - 978-3-319-43587-9
T3 - E X S
SP - 81
EP - 126
BT - AMP-activated Protein Kinase
A2 - Cordero, M D
A2 - Viollet, B
PB - Springer
ER -
ID: 168911648