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