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  • Artikel: DFG Deutsche Nationallizenzen  (2)
  • Type 2 (non-insulin-dependent) diabetes  (2)
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  • Artikel: DFG Deutsche Nationallizenzen  (2)
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  • 1
    ISSN: 1432-0428
    Schlagwort(e): 3-3H-glucose ; primed-continuous tracer technique ; Type 2 (non-insulin-dependent) diabetes ; basal glucose turnover ; glucose appearance ; glucose disappearance ; steady-state conditions ; Steele's equations
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Using primed-continuous 3-3H-glucose infusion, basal glucose production rate has been reported to be 140% higher than normal or almost normal in hyperglycaemic patients with Type 2 (non-insulin-dependent) diabetes mellitus. To determine whether these markedly different results could be due to the mode of priming: fixed or adjusted, or the mode of calculation: steady state or non-steady state equations, we studied 11 patients with Type 2 diabetes (fasting plasma glucose 8–20 mmol/l). For 6 h 3-3H-glucose (0.40 μCi/min) was infused preceded by a priming dose of 40 μCi (fixed priming), or 40 μCi · plasma glucose (mmol/l)·5−1 (adjusted priming). In diabetic patients the plasma glucose concentration was not constant but declined 0.52±0.07 mmol·l−1· h−1. Furthermore, the rate of fall was correlated to the fasting plasma glucose concentration (r=0.90, p〈0.01). Thus, the fasting state was not a steady state condition. Using adjusted priming a constant tracer steady state level was obtained within 60 min. In contrast, using fixed priming tracer steady state was not reached within 6 h. The initial tracer level was far below, and increased in time towards the steady state level observed after adjusted priming. Consequently, using Steele's equations after fixed priming, glucose production rates calculated after 90–120 min were overestimated in proportion to fasting hyperglycaemia. In conclusion: The fasting state in patients with Type 2 diabetes is not a steady state condition. Adjusted priming seems most appropriate in Type 2 diabetes. By estimating glucose production 2 h after fixed priming or assuming steady state conditions, most previous studies may have overestimated basal glucose production in Type 2 diabetes in proportion to fasting hyperglycaemia.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    ISSN: 1432-0428
    Schlagwort(e): Type 2 (non-insulin-dependent) diabetes ; obesity ; insulin resistance ; non-oxidative glucose metabolism ; skeletal muscle ; glycogen synthase
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary In order to evaluate the importance of a defect in insulin mediated non-oxidative glucose metabolism and glycogen synthase activity in skeletal muscles in obese subjects with and without Type 2 (non-insulin-dependent) diabetes mellitus we studied: 10 lean and 10 obese control subjects and 12 obese diabetic patients using the euglycaemic hyperinsulinaemic clamp technique (basal, 20 mU · (m2)−1 · min−1, 80mU·(m2)−1·min−1) in combination with indirect calorimetry. Muscle biopsies were taken from m. vastus lateralis at each insulin level. We found that non-oxidative glucose metabolism could be stimulated by insulin in all three groups (p〈0.01). The values obtained at the highest insulin levels (around 140 μU/ml) were lower in both obese groups compared to the lean control subjects (118±21, 185±31, 249±14 mg·(m2)−1·min−1 (p〈 0.01)). Insulin stimulation of the glycogen synthase activity at a glucose-6-phosphate concentration of 0.1 mmol/l was absent in both obese groups, while activities increased significantly in the lean control subjects (19.6±4.2% to 45.6±6.8%, p〈 0.01). Glycogen synthase activities at the highest insulin concentrations only differed significantly between lean control subjects and obese diabetic patients (45±7% and 31±5%, p〈 0.05). We conclude that insulin resistance in peripheral tissues in obese subjects with and without Type 2 diabetes may be partly explained by a reduced insulin mediated non-oxidative glucose metabolism and that this abnormality might be due to an absent insulin stimulation of glycogen synthase in skeletal muscles. This enzyme defect is correlated to obesity itself.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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