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  • 1
    Electronic Resource
    Electronic Resource
    Decreased tyrosine kinase activity in partially purified insulin receptors from muscle of young, non-obese first degree relatives of patients with Type 2 (non-insulin-dependent) diabetes mellitus (1993)
    Springer
    Diabetologia 36 (1993), S. 668-674 
    Details
    ISSN: 1432-0428
    Keywords: Insulin resistance ; insulin receptor ; tyrosine kinase ; skeletal muscle ; Type 2 (non-insulin-dependent) diabetes mellitus ; insulin binding
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recently, we demonstrated insulin resistance due to reduced glucose storage in young relatives of Type 2 diabetic patients. To investigate whether this was associated with a defective insulin receptor kinase, we studied ten of these young (27±1 years old) non-obese glucose tolerant first degree relatives of patients with Type 2 diabetes and eight matched control subjects with no family history of diabetes. Insulin sensitivity was assessed by a hyperinsulinaemic, euglycaemic clamp. Insulin receptors were partially purified from muscle biopsies obtained in the basal and the insulin-stimulated state during the clamp. Insulin binding capacity was decreased by 28% in the relatives (p〈0.05) in the basal biopsy. Tyrosine kinase activity in the receptor preparation was decreased by 50% in both basal and insulin-stimulated biopsies from the relatives. After stimulation with insulin “in vitro”, kinase activity was reduced in the relatives in basal (p〈0.005) and insulin-stimulated (p〈0.01) biopsies and also when expressed per insulin binding capacity (p≈0.05). Insulin stimulation of non-oxidative glucose metabolism correlated with “in vitro” insulin-stimulated tyrosine kinase activity (r=0.61, p〈0.01) and also when expressed per binding capacity (r=0.53, p〈0.025). We suggest that the marked defect in tyrosine kinase activity in partially purified insulin receptors from skeletal muscle is an early event in the development of insulin resistance and contributes to the pathophysiology of Type 2 diabetes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404079
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Expression of insulin regulatable glucose transporters in skeletal muscle from Type 2 (non-insulin-dependent) diabetic patients (1990)
    Springer
    Diabetologia 33 (1990), S. 625-627 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes mellitus ; skeletal muscle ; glucose transporters ; insulin regulatable glucose transporters
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A prominent feature of Type 2 (non-insulin-dependent) diabetes mellitus is the inability of insulin to appropiately increase the transport of glucose into target tissue. In adipocytes from individuals with Type 2 diabetes, insulin resistance has been shown to be associated with a depletion of glucose transporters. Similarly, streptozotocin induced diabetes causes a diminished expression of the insulin regulatable glucose transporter in rat adipocytes. The expression of this glucose transporter isoform has not yet been investigated in muscle tissue from patients with Type 2 diabetes. We have measured the content of the insulin regulatable glucose transporter in a vesicular fraction isolated from muscle biopsies from fasting individuals with Type 2 diabetes and control subjects, and we found that the number of the insulin regulatable glucose transporters expressed in skeletal muscle was unaffected by Type 2 diabetes (0.208 vs 0.205, arbitrary units, p〉0.5, control subjects and diabetic patients). Thus, the decreased glucose disposal in Type 2 diabetes is not associated with a diminished number of insulin regulatable glucose transporters.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400207
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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