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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 14 (1978), S. 337-341 
    ISSN: 1432-0428
    Keywords: Injury ; insulin binding ; insulin resistance ; glucagon binding ; muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Acute insulin resistance developed after scald injury in the mouse. After 2h plasma glucose and insulin concentrations were each raised about two-fold. Glucose metabolism was studied in vitro in soleus muscles isolated at this time. Glycolysis and glycogen synthesis, and their stimulation by insulin, were unchanged in muscles from scalded mice, and insulin-stimulated transport of 2-deoxyglucose slightly increased, showing that the insulin resistance seen in vivo is not maintained in isolated tissues. Binding of insulin to liver cell membranes prepared from scalded mice was unaltered, whilst that of glucagon was slightly but significantly reduced, showing that changes in polypeptide-hormone receptors can occur within this short time. It was concluded that the acute loss of sensitivity to insulin after injury does not result from a change in insulin receptor sites and presumably reflects an impairment of glucose metabolism in vivo mediated by circulating hormones.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Insulin receptor ; tyrosine kinase ; goldthioglucose obese mice ; insulin resistance ; muscle ; hyperinsulinaemia ; acarbose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of prolonged treatment with acarbose, an inhibitor of α-glycosidase, has been studied in mice made obese and hyperinsulinaemic by goldthioglucose. After the onset of obesity, one month after goldthioglucose administration, mice were then treated, with or without a 10% sucrose supplement, for four months with acarbose, added to the diet at 50 mg/100 g food. When mice received a standard diet, acarbose had no effect on body weight, blood glucose or insulin levels. In contrast, in the control obese mice receiving a 10% sucrose-enriched diet, it decreased the body weight gain, and prevented the rise in glycaemia and insulinaemia. Basal (non insulin-stimulated) glucose uptake, which is decreased in isolated soleus muscle from untreated obese mice, returned to normal values under acarbose treatment. However, muscle insulin resistance was not improved in acarbose-treated obese mice at maximal and submaximal effective concentrations, despite a higher insulin binding in muscles of acarbose-treated obese than in control obese animals. Furthermore, insulin receptor autophosphorylation and tyrosine kinase activity were altered similarly in treated and untreated obese mice compared to lean mice.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Insulin resistance ; experimental obesity ; phosphotyrosine phosphatase ; muscle ; liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To study the possible involvement of phosphotyrosine phosphatases in insulin resistance, the ability of cytosolic and membrane preparations to dephosphorylate insulin receptors was examined in lean and goldthioglucose-treated insulin-resistant and obese mice. Preparations were obtained from liver, heart, diaphragm and hindleg muscle and their phosphotyrosine phosphatase activities were measured using an immunoenzymatic assay with phosphorylated insulin receptors as substrate. Liver cytosolic and particulate phosphotyrosine phosphatases were more potent than preparations from other tissues and were able to almost completely dephosphorylate the insulin receptor in a dose- and time-dependent manner. No change was observed in cytosolic and membrane-associated phosphotyrosine phosphatases in liver, diaphragm, and heart of obese mice compared with lean mice. In contrast, cytosolic, but not membrane-associated, phosphotyrosine phosphatase activity was decreased in hindleg muscles of obese mice. These results suggest that the regulation of phosphotyrosine phosphatases is tissue-specific. In addition, alterations in total phosphotyrosine phosphatase activity do not appear to play an important role in insulin resistance in all tissues of obese mice, although specific changes cannot be excluded.
    Type of Medium: Electronic Resource
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