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, Jesper Bratz Birk, Sara Gry Vienberg, B Andersen, Henning Beck-Nielsen, Jørgen Wojtaszewski, Kurt Højlund

    30 Citationer (Scopus)

    Abstract

    AIMS/HYPOTHESIS: 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. METHODS: Whole-body glucose metabolism was studied in 12 patients with type 2 diabetes, and 10 lean and 10 obese non-diabetic controls by means of indirect calorimetry and tracers during a euglycaemic-hyperinsulinaemic clamp. The diabetic patients underwent a second isoglycaemic-hyperinsulinaemic clamp maintaining fasting hyperglycaemia. Muscle biopsies from m. vastus lateralis were obtained before and after the clamp for examination of GS and relevant insulin signalling components. RESULTS: During euglycaemia, insulin-stimulated glucose disposal, glucose oxidation and non-oxidative glucose metabolism were reduced in the diabetic group compared with both control groups (p¿
    OriginalsprogEngelsk
    TidsskriftDiabetologia
    Vol/bind55
    Udgave nummer5
    Sider (fra-til)1435-1445
    Antal sider11
    ISSN0012-186X
    DOI
    StatusUdgivet - maj 2012

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