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  • 1
    Electronic Resource
    Electronic Resource
    Effects of glycaemia on glucose transport in isolated skeletal muscle from patients with NIDDM: in vitro reversal of muscular insulin resistance (1994)
    Springer
    Diabetologia 37 (1994), S. 270-277 
    Details
    ISSN: 1432-0428
    Keywords: Glucose transport ; glucose kinetics ; human skeletal muscle ; insulin action ; insulin resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the influence of altered glucose levels on insulin-stimulated 3-0-methylglucose transport in isolated skeletal muscle obtained from NIDDM patients (n=13) and non-diabetic subjects (n=23). Whole body insulin sensitivity was 71% lower in the NIDDM patients compared to the non-diabetic subjects (p 〈0.05), whereas, insulin-mediated peripheral glucose utilization in the NIDDM patients under hyperglycaemic conditions was comparable to that of the non-diabetic subjects at euglycaemia. Following a 30-min in vitro exposure to 4 mmol/l glucose, insulin-stimulated 3-0-methylglucose transport (600 pmol/l insulin) was 40% lower in isolated skeletal muscle strips from the NIDDM patients when compared to muscle strips from the non-diabetic subjects. The impaired capacity for insulin-stimulated 3-0-methylglucose transport in the NIDDM skeletal muscle was normalized following prolonged (2 h) exposure to 4 mmol/l, but not to 8 mmol/l glucose. Insulin-stimulated 3-0-methylglucose transport in the NIDDM skeletal muscle exposed to 8 mmol/l glucose was similar to that of the non-diabetic muscle exposed to 5 mmol/l glucose, but was decreased by 43% (p 〈0.01) when compared to non-diabetic muscle exposed to 8 mmol/l glucose. Despite the impaired insulin-stimulated 3-0-methylglucose transport capacity demonstrated by skeletal muscle from the NIDDM patients, skeletal muscle glycogen content was similar to that of the non-diabetic subjects. Kinetic studies revel a Km for 3-0-methylglucose transport of 9.7 and 8.8 mmol/l glucose for basal and insulin-stimulated conditions, respectively. In conclusion, the impaired capacity for insulinstimulated glucose transport in skeletal muscle from patients with NIDDM appears to protect the cell from excessive glucose uptake under hyperglycaemic conditions. Furthermore, the in vitro normalization of the decreased insulin-stimulated glucose transport in NIDDM skeletal muscle following exposure to 4 mmol/l glucose suggests that glycaemia per se has a profound effect on the regulation of muscular glucose transport.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00398054
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    C-peptide stimulates glucose transport in isolated human skeletal muscle independent of insulin receptor and tyrosine kinase activation (1996)
    Springer
    Diabetologia 39 (1996), S. 306-313 
    Details
    ISSN: 1432-0428
    Keywords: Glucose transport ; insulin receptor ; insulin binding ; insulin receptor tyrosine kinase ; human skeletal muscle ; C-peptide ; insulin ; catecholamines ; insulin-dependent diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have previously demonstrated that C-peptide stimulates glucose transport in skeletal muscle from non-diabetic subjects in a dose-dependent manner. To further elucidate the mechanism by which C-peptide activates glucose transport, we investigated the influence of human recombinant C-peptide on receptor and post-receptor events involved in the glucose transport process. Human skeletal muscle specimens were obtained from the vastus lateralis by means of an open biopsy procedure. Stimulation of isolated muscle strips from healthy control subjects with supra-physiological concentrations of insulin (6,000 pmol/l) and C-peptide (2,500 pmol/l), did not further augment the twofold increase in the rate of 3-o-methylglucose transport induced by either stimulus alone. C-peptide did not displace 125I-insulin binding from partially purified receptors, nor did it activate receptor tyrosine kinase activity. Tyrosine-labelled 125I-C-peptide did not bind specifically to crude membranes prepared from skeletal muscle, or to any serum protein other than albumin. The Β-adrenergic receptor stimulation with isoproterenol inhibited insulin- but not C-peptide-mediated 3-o-methylglucose transport by 63±18% (p〈0.01), whereas the cyclic AMP analogue, Bt2cAMP, abolished the insulin- and C-peptide-stimulated 3-o-methylglucose transport. C-peptide (600 pmol/l) increased 3-o-methylglucose transport 1.8±0.2-fold in skeletal muscle specimens from patients with insulin-dependent diabetes mellitus. In conclusion, C-peptide stimulates glucose transport by a mechanism independent of insulin receptor and tyrosine kinase activation. In contrast to the effect on insulin-stimulated glucose transport, catecholamines do not appear to have a counter regulatory action on C-peptide-mediated glucose transport.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418346
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of non-esterified fatty acids on insulin-stimulated glucose transport in isolated skeletal muscle from patients with type 2 (non-insulin-dependent) diabetes mellitus (1994)
    Springer
    Acta diabetologica 31 (1994), S. 169-172 
    Details
    ISSN: 1432-5233
    Keywords: Glucose transport ; Human skeletal muscle ; Non-esterified fatty acids ; Insulin action ; Insulin resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The influence of elevated levels of oleate on insulin-stimulated 3-0-methylglucose transport was assessed in vitro, in isolated skeletal muscle obtained from patients with type 2 (non-insulin-dependent) diabetes mellitus (n=7) and control subjects (n=8). An increase in oleate levels from 0.3 to 1.0 mmol/l induced a 3.7-fold increase in the rate of oleate oxidation (P〈0.001) in skeletal muscle from control subjects. However, the rate of insulinstimulated 3-0-methylglucose transport was not altered in isolated skeletal muscle from the control subjects or the type 2 diabetic patients following exposure to 1.0 mmol/l oleate. This observation indicates that elevation of nonesterified fatty acids to a high physiological level has no inhibitory effect on glucose transport.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00570374
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    Paper (German National Licenses)
    Fulltext
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