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Hvidovre Hospital - en del af Københavns Universitetshospital
Udgivet

Mechanisms underlying absent training-induced improvement in insulin action in lean, hyperandrogenic women with polycystic ovary syndrome

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  • Solvejg L Hansen
  • Kirstine N Bojsen-Møller
  • Anne-Marie Lundsgaard
  • Frederikke L Hendrich
  • Lisbeth Nilas
  • Kim A Sjøberg
  • Janne R Hingst
  • Annette K Serup
  • Carlos Henríquez-Olguín
  • Christian S Carl
  • Louise F Wernblad
  • Marie Henneberg
  • Katja M Lustrup
  • Christine Hansen
  • Thomas E Jensen
  • Sten Madsbad
  • Jørgen F P Wojtaszewski
  • Erik A Richter
  • Bente Kiens
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Women with polycystic ovary syndrome (PCOS) have been shown to be less insulin sensitive compared with control (CON) women, independent of BMI. Training is associated with molecular adaptations in skeletal muscle, improving glucose uptake and metabolism in both healthy individuals and patients with type 2 diabetes. In the current study, lean hyperandrogenic women with PCOS ( n = 9) and healthy CON women ( n = 9) completed 14 weeks of controlled and supervised exercise training. In CON, the training intervention increased whole-body insulin action by 26% and insulin-stimulated leg glucose uptake by 53% together with increased insulin-stimulated leg blood flow and a more oxidative muscle fiber type distribution. In PCOS, no such changes were found, despite similar training intensity and improvements in VO 2max In skeletal muscle of CON but not PCOS, training increased GLUT4 and HKII mRNA and protein expressions. These data suggest that the impaired increase in whole-body insulin action in women with PCOS with training is caused by an impaired ability to upregulate key glucose-handling proteins for insulin-stimulated glucose uptake in skeletal muscle and insulin-stimulated leg blood flow. Still, other important benefits of exercise training appeared in women with PCOS, including an improvement of the hyperandrogenic state.

OriginalsprogEngelsk
TidsskriftDiabetes
Vol/bind69
Udgave nummer11
Sider (fra-til)2267-2280
Antal sider14
ISSN0012-1797
DOI
StatusUdgivet - nov. 2020

Bibliografisk note

© 2020 by the American Diabetes Association.

ID: 60882672