Hyperglycaemia normalises insulin action on glucose metabolism but not the impaired activation of AKT and glycogen synthase in the skeletal muscle of patients with type 2 diabetes

B F Vind, J B Birk, Sara Gry Vienberg, B Andersen, H Beck-Nielsen, Jørgen Wojtaszewski, K Højlund

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Abstrakt

In type 2 diabetes, reduced insulin-stimulated glucose disposal, primarily glycogen synthesis, is associated with defective insulin activation of glycogen synthase (GS) in skeletal muscle. Hyperglycaemia may compensate for these defects, but to what extent it involves improved insulin signalling to glycogen synthesis remains to be clarified.
OriginalsprogEngelsk
TidsskriftDiabetologia
Vol/bind55
Udgave nummer5
Sider (fra-til)1435-45
Antal sider11
ISSN0012-186X
DOI
StatusUdgivet - 2012

Fingeraftryk Dyk ned i forskningsemnerne om 'Hyperglycaemia normalises insulin action on glucose metabolism but not the impaired activation of AKT and glycogen synthase in the skeletal muscle of patients with type 2 diabetes'. Sammen danner de et unikt fingeraftryk.

  • Citationsformater