Intact regulation of the AMPK signaling network in response to exercise and insulin in skeletal muscle of male patients with type 2 diabetes: Illumination of AMPK activation in recovery from exercise

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Standard

Intact regulation of the AMPK signaling network in response to exercise and insulin in skeletal muscle of male patients with type 2 diabetes : Illumination of AMPK activation in recovery from exercise. / Kjøbsted, Rasmus; Pedersen, Andreas J T; Hingst, Janne R; Sabaratnam, Rugivan; Birk, Jesper Bratz; Kristensen, Jonas Møller; Højlund, Kurt; Wojtaszewski, Jørgen.

I: Diabetes, Bind 65, Nr. 5, 2016, s. 1219-1230.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Kjøbsted, R, Pedersen, AJT, Hingst, JR, Sabaratnam, R, Birk, JB, Kristensen, JM, Højlund, K & Wojtaszewski, J 2016, 'Intact regulation of the AMPK signaling network in response to exercise and insulin in skeletal muscle of male patients with type 2 diabetes: Illumination of AMPK activation in recovery from exercise', Diabetes, bind 65, nr. 5, s. 1219-1230. https://doi.org/10.2337/db15-1034

APA

Kjøbsted, R., Pedersen, A. J. T., Hingst, J. R., Sabaratnam, R., Birk, J. B., Kristensen, J. M., ... Wojtaszewski, J. (2016). Intact regulation of the AMPK signaling network in response to exercise and insulin in skeletal muscle of male patients with type 2 diabetes: Illumination of AMPK activation in recovery from exercise. Diabetes, 65(5), 1219-1230. https://doi.org/10.2337/db15-1034

Vancouver

Kjøbsted R, Pedersen AJT, Hingst JR, Sabaratnam R, Birk JB, Kristensen JM o.a. Intact regulation of the AMPK signaling network in response to exercise and insulin in skeletal muscle of male patients with type 2 diabetes: Illumination of AMPK activation in recovery from exercise. Diabetes. 2016;65(5):1219-1230. https://doi.org/10.2337/db15-1034

Author

Kjøbsted, Rasmus ; Pedersen, Andreas J T ; Hingst, Janne R ; Sabaratnam, Rugivan ; Birk, Jesper Bratz ; Kristensen, Jonas Møller ; Højlund, Kurt ; Wojtaszewski, Jørgen. / Intact regulation of the AMPK signaling network in response to exercise and insulin in skeletal muscle of male patients with type 2 diabetes : Illumination of AMPK activation in recovery from exercise. I: Diabetes. 2016 ; Bind 65, Nr. 5. s. 1219-1230.

Bibtex

@article{8f134b8c9ff14743a62a1430faa81838,
title = "Intact regulation of the AMPK signaling network in response to exercise and insulin in skeletal muscle of male patients with type 2 diabetes: Illumination of AMPK activation in recovery from exercise",
abstract = "Current evidence on exercise-mediated AMPK regulation in skeletal muscle of type 2 diabetic (T2D) patients is inconclusive. This may relate to inadequate segregation of trimer complexes in the investigation of AMPK activity. We examined the regulation of AMPK and downstream targets ACCβ, TBC1D1 and TBC1D4 in muscle biopsies obtained from thirteen overweight/obese T2D and fourteen weight-matched control male subjects before, immediately after and 3 h after exercise. Exercise increased AMPK α2β2γ3 activity and phosphorylation of ACCβ Ser(221), TBC1D1 Ser(237)/Thr(596) and TBC1D4 Ser(704). Conversely, exercise decreased AMPK α1β2γ1 activity and TBC1D4 Ser(318)/Thr(642) phosphorylation. Interestingly, compared to pre-exercise, 3 h into exercise recovery AMPK α2β2γ1 and α1β2γ1 activity were increased concomitant with increased TBC1D4 Ser(318)/Ser(341)/Ser(704) phosphorylation. No differences in these responses were observed between T2D and control subjects. Subjects were also studied by euglycemic-hyperinsulinemic clamps performed at rest and 3 h after exercise. We found no evidence for insulin to regulate AMPK activity. Thus, in muscle of T2D patients AMPK signaling is not compromised during exercise and insulin stimulation. Our results reveal a hitherto unrecognized activation of specific AMPK complexes in exercise recovery. We hypothesize that the differential regulation of AMPK complexes plays an important role for muscle metabolism and adaptations to exercise.",
author = "Rasmus Kj{\o}bsted and Pedersen, {Andreas J T} and Hingst, {Janne R} and Rugivan Sabaratnam and Birk, {Jesper Bratz} and Kristensen, {Jonas M{\o}ller} and Kurt H{\o}jlund and J{\o}rgen Wojtaszewski",
note = "CURIS 2016 NEXS 110",
year = "2016",
doi = "10.2337/db15-1034",
language = "English",
volume = "65",
pages = "1219--1230",
journal = "Diabetes",
issn = "0012-1797",
publisher = "American Diabetes Association",
number = "5",

}

RIS

TY - JOUR

T1 - Intact regulation of the AMPK signaling network in response to exercise and insulin in skeletal muscle of male patients with type 2 diabetes

T2 - Illumination of AMPK activation in recovery from exercise

AU - Kjøbsted, Rasmus

AU - Pedersen, Andreas J T

AU - Hingst, Janne R

AU - Sabaratnam, Rugivan

AU - Birk, Jesper Bratz

AU - Kristensen, Jonas Møller

AU - Højlund, Kurt

AU - Wojtaszewski, Jørgen

N1 - CURIS 2016 NEXS 110

PY - 2016

Y1 - 2016

N2 - Current evidence on exercise-mediated AMPK regulation in skeletal muscle of type 2 diabetic (T2D) patients is inconclusive. This may relate to inadequate segregation of trimer complexes in the investigation of AMPK activity. We examined the regulation of AMPK and downstream targets ACCβ, TBC1D1 and TBC1D4 in muscle biopsies obtained from thirteen overweight/obese T2D and fourteen weight-matched control male subjects before, immediately after and 3 h after exercise. Exercise increased AMPK α2β2γ3 activity and phosphorylation of ACCβ Ser(221), TBC1D1 Ser(237)/Thr(596) and TBC1D4 Ser(704). Conversely, exercise decreased AMPK α1β2γ1 activity and TBC1D4 Ser(318)/Thr(642) phosphorylation. Interestingly, compared to pre-exercise, 3 h into exercise recovery AMPK α2β2γ1 and α1β2γ1 activity were increased concomitant with increased TBC1D4 Ser(318)/Ser(341)/Ser(704) phosphorylation. No differences in these responses were observed between T2D and control subjects. Subjects were also studied by euglycemic-hyperinsulinemic clamps performed at rest and 3 h after exercise. We found no evidence for insulin to regulate AMPK activity. Thus, in muscle of T2D patients AMPK signaling is not compromised during exercise and insulin stimulation. Our results reveal a hitherto unrecognized activation of specific AMPK complexes in exercise recovery. We hypothesize that the differential regulation of AMPK complexes plays an important role for muscle metabolism and adaptations to exercise.

AB - Current evidence on exercise-mediated AMPK regulation in skeletal muscle of type 2 diabetic (T2D) patients is inconclusive. This may relate to inadequate segregation of trimer complexes in the investigation of AMPK activity. We examined the regulation of AMPK and downstream targets ACCβ, TBC1D1 and TBC1D4 in muscle biopsies obtained from thirteen overweight/obese T2D and fourteen weight-matched control male subjects before, immediately after and 3 h after exercise. Exercise increased AMPK α2β2γ3 activity and phosphorylation of ACCβ Ser(221), TBC1D1 Ser(237)/Thr(596) and TBC1D4 Ser(704). Conversely, exercise decreased AMPK α1β2γ1 activity and TBC1D4 Ser(318)/Thr(642) phosphorylation. Interestingly, compared to pre-exercise, 3 h into exercise recovery AMPK α2β2γ1 and α1β2γ1 activity were increased concomitant with increased TBC1D4 Ser(318)/Ser(341)/Ser(704) phosphorylation. No differences in these responses were observed between T2D and control subjects. Subjects were also studied by euglycemic-hyperinsulinemic clamps performed at rest and 3 h after exercise. We found no evidence for insulin to regulate AMPK activity. Thus, in muscle of T2D patients AMPK signaling is not compromised during exercise and insulin stimulation. Our results reveal a hitherto unrecognized activation of specific AMPK complexes in exercise recovery. We hypothesize that the differential regulation of AMPK complexes plays an important role for muscle metabolism and adaptations to exercise.

U2 - 10.2337/db15-1034

DO - 10.2337/db15-1034

M3 - Journal article

C2 - 26822091

VL - 65

SP - 1219

EP - 1230

JO - Diabetes

JF - Diabetes

SN - 0012-1797

IS - 5

ER -

ID: 154803848