Is the Glucose Disappearance Rate Reduced in TD

Glucose disappears into skeletal muscle, fat tissue and liver, mediated by insulin, and into the central nervous system, blood cells and several other tissues mediated by the mass action of glucose itself. The insulin-mediated glucose uptake in skeletal muscle is significantly reduced in T2D subjects due to a reduced glycogen synthesis and glucose oxidation (Fig. 2) [11]. Since most glucose after a meal is taken up in skeletal muscle, the defect in insulin action adds to the degree of postprandial

Plasma insulin (mU/L)

Fig. 2. Dose-response effects of insulin on glucose disposal (Rd) and HGP in T2D patients with fasting hyperinsuli-naemia (closed symbols) and in age- and weight-matched control subjects (open symbols). *p < 0.05 [9].

Plasma insulin (mU/L)

Fig. 2. Dose-response effects of insulin on glucose disposal (Rd) and HGP in T2D patients with fasting hyperinsuli-naemia (closed symbols) and in age- and weight-matched control subjects (open symbols). *p < 0.05 [9].

hyperglycaemia. Thus, insulin resistance plays an important role in postprandial blood glucose values [12]. Improvement of insulin action in T2D subjects must therefore be a primary aim for the normalisation of blood glucose values, mainly in the postprandial state. Normalisation of insulin sensitivity in peripheral tissues in T2D has, however, never been the main objective, as we possessed no tools carrying the potential for reaching this objective. However, the recently discovered PPAR (peroxisome proliferator-activated receptor) gamma agonists, namely glitazones, carry this potential.

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