AMPKγ3 Controls Muscle Glucose Uptake in Recovery From Exercise to Recapture Energy Stores

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

AMPKγ3 Controls Muscle Glucose Uptake in Recovery From Exercise to Recapture Energy Stores. / Kido, Kohei; Eskesen, Nicolas O.; Henriksen, Nicolai S.; Onslev, Johan; Kristensen, Jonas M.; Larsen, Magnus R.; Hingst, Janne R.; Knudsen, Jonas R.; Birk, Jesper B.; Andersen, Nicoline R.; Jensen, Thomas E.; Pehmoller, Christian; Wojtaszewski, Jørgen F.P.; Kjøbsted, Rasmus.

In: Diabetes, Vol. 72, No. 10, 2023, p. 1397-1408.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Kido, K, Eskesen, NO, Henriksen, NS, Onslev, J, Kristensen, JM, Larsen, MR, Hingst, JR, Knudsen, JR, Birk, JB, Andersen, NR, Jensen, TE, Pehmoller, C, Wojtaszewski, JFP & Kjøbsted, R 2023, 'AMPKγ3 Controls Muscle Glucose Uptake in Recovery From Exercise to Recapture Energy Stores', Diabetes, vol. 72, no. 10, pp. 1397-1408. https://doi.org/10.2337/db23-0358

APA

Kido, K., Eskesen, N. O., Henriksen, N. S., Onslev, J., Kristensen, J. M., Larsen, M. R., Hingst, J. R., Knudsen, J. R., Birk, J. B., Andersen, N. R., Jensen, T. E., Pehmoller, C., Wojtaszewski, J. F. P., & Kjøbsted, R. (2023). AMPKγ3 Controls Muscle Glucose Uptake in Recovery From Exercise to Recapture Energy Stores. Diabetes, 72(10), 1397-1408. https://doi.org/10.2337/db23-0358

Vancouver

Kido K, Eskesen NO, Henriksen NS, Onslev J, Kristensen JM, Larsen MR et al. AMPKγ3 Controls Muscle Glucose Uptake in Recovery From Exercise to Recapture Energy Stores. Diabetes. 2023;72(10):1397-1408. https://doi.org/10.2337/db23-0358

Author

Kido, Kohei ; Eskesen, Nicolas O. ; Henriksen, Nicolai S. ; Onslev, Johan ; Kristensen, Jonas M. ; Larsen, Magnus R. ; Hingst, Janne R. ; Knudsen, Jonas R. ; Birk, Jesper B. ; Andersen, Nicoline R. ; Jensen, Thomas E. ; Pehmoller, Christian ; Wojtaszewski, Jørgen F.P. ; Kjøbsted, Rasmus. / AMPKγ3 Controls Muscle Glucose Uptake in Recovery From Exercise to Recapture Energy Stores. In: Diabetes. 2023 ; Vol. 72, No. 10. pp. 1397-1408.

Bibtex

@article{8a6bc18b64c44529a64d3d75dc470f52,
title = "AMPKγ3 Controls Muscle Glucose Uptake in Recovery From Exercise to Recapture Energy Stores",
abstract = "Exercise increases muscle glucose uptake independently of insulin signaling and represents a cornerstone for the prevention ofmetabolic disorders. Pharmacological activation of the exercise-responsive AMPK in skeletal muscle has been proven successful as a therapeutic approach to treat metabolic disorders by improving glucose homeostasis through the regulation of muscle glucose uptake. However, conflicting observations cloud the proposed role of AMPK as a necessary regulator of muscle glucose uptake during exercise.We show that glucose uptake increases in human skeletal muscle in the absence of AMPK activation during exercise and that exercise-stimulated AMPKγ3 activity strongly correlates to muscle glucose uptake in the postexercise period. In AMPKγ3-deficient mice, muscle glucose uptake is normally regulated during exercise and contractions but impaired in the recovery period from these stimuli. Impaired glucose uptake in recovery fromexercise and contractions is associated with a lower glucose extraction, which can be explained by a diminished permeability to glucose and abundance of GLUT4 at the muscle plasmamembrane. As a result, AMPKγ3deficiency impairs muscle glycogen resynthesis following exercise. These results identify a physiological function of the AMPKγ3 complex in human and rodent skeletal muscle that regulates glucose uptake in recovery from exercise to recapture muscle energy stores.",
author = "Kohei Kido and Eskesen, {Nicolas O.} and Henriksen, {Nicolai S.} and Johan Onslev and Kristensen, {Jonas M.} and Larsen, {Magnus R.} and Hingst, {Janne R.} and Knudsen, {Jonas R.} and Birk, {Jesper B.} and Andersen, {Nicoline R.} and Jensen, {Thomas E.} and Christian Pehmoller and Wojtaszewski, {J{\o}rgen F.P.} and Rasmus Kj{\o}bsted",
note = "Publisher Copyright: {\textcopyright} 2023 by the American Diabetes Association.",
year = "2023",
doi = "10.2337/db23-0358",
language = "English",
volume = "72",
pages = "1397--1408",
journal = "Diabetes",
issn = "0012-1797",
publisher = "American Diabetes Association",
number = "10",

}

RIS

TY - JOUR

T1 - AMPKγ3 Controls Muscle Glucose Uptake in Recovery From Exercise to Recapture Energy Stores

AU - Kido, Kohei

AU - Eskesen, Nicolas O.

AU - Henriksen, Nicolai S.

AU - Onslev, Johan

AU - Kristensen, Jonas M.

AU - Larsen, Magnus R.

AU - Hingst, Janne R.

AU - Knudsen, Jonas R.

AU - Birk, Jesper B.

AU - Andersen, Nicoline R.

AU - Jensen, Thomas E.

AU - Pehmoller, Christian

AU - Wojtaszewski, Jørgen F.P.

AU - Kjøbsted, Rasmus

N1 - Publisher Copyright: © 2023 by the American Diabetes Association.

PY - 2023

Y1 - 2023

N2 - Exercise increases muscle glucose uptake independently of insulin signaling and represents a cornerstone for the prevention ofmetabolic disorders. Pharmacological activation of the exercise-responsive AMPK in skeletal muscle has been proven successful as a therapeutic approach to treat metabolic disorders by improving glucose homeostasis through the regulation of muscle glucose uptake. However, conflicting observations cloud the proposed role of AMPK as a necessary regulator of muscle glucose uptake during exercise.We show that glucose uptake increases in human skeletal muscle in the absence of AMPK activation during exercise and that exercise-stimulated AMPKγ3 activity strongly correlates to muscle glucose uptake in the postexercise period. In AMPKγ3-deficient mice, muscle glucose uptake is normally regulated during exercise and contractions but impaired in the recovery period from these stimuli. Impaired glucose uptake in recovery fromexercise and contractions is associated with a lower glucose extraction, which can be explained by a diminished permeability to glucose and abundance of GLUT4 at the muscle plasmamembrane. As a result, AMPKγ3deficiency impairs muscle glycogen resynthesis following exercise. These results identify a physiological function of the AMPKγ3 complex in human and rodent skeletal muscle that regulates glucose uptake in recovery from exercise to recapture muscle energy stores.

AB - Exercise increases muscle glucose uptake independently of insulin signaling and represents a cornerstone for the prevention ofmetabolic disorders. Pharmacological activation of the exercise-responsive AMPK in skeletal muscle has been proven successful as a therapeutic approach to treat metabolic disorders by improving glucose homeostasis through the regulation of muscle glucose uptake. However, conflicting observations cloud the proposed role of AMPK as a necessary regulator of muscle glucose uptake during exercise.We show that glucose uptake increases in human skeletal muscle in the absence of AMPK activation during exercise and that exercise-stimulated AMPKγ3 activity strongly correlates to muscle glucose uptake in the postexercise period. In AMPKγ3-deficient mice, muscle glucose uptake is normally regulated during exercise and contractions but impaired in the recovery period from these stimuli. Impaired glucose uptake in recovery fromexercise and contractions is associated with a lower glucose extraction, which can be explained by a diminished permeability to glucose and abundance of GLUT4 at the muscle plasmamembrane. As a result, AMPKγ3deficiency impairs muscle glycogen resynthesis following exercise. These results identify a physiological function of the AMPKγ3 complex in human and rodent skeletal muscle that regulates glucose uptake in recovery from exercise to recapture muscle energy stores.

U2 - 10.2337/db23-0358

DO - 10.2337/db23-0358

M3 - Journal article

C2 - 37506328

AN - SCOPUS:85171901498

VL - 72

SP - 1397

EP - 1408

JO - Diabetes

JF - Diabetes

SN - 0012-1797

IS - 10

ER -

ID: 372474164