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  • 1
    Electronic Resource
    Electronic Resource
    The development of hyperglycaemia in patients with insulin-resistant generalized lipoatrophic syndromes (1993)
    Springer
    Diabetologia 36 (1993), S. 1288-1292 
    Details
    ISSN: 1432-0428
    Keywords: Generalized lipoatrophic diabetes ; insulin resistance ; hyperinsulinaemic euglycaemic clamp ; stable isotope labelled glucose ; hepatic glucose production
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insulin resistance is present in patients suffering from lipoatrophic syndromes long before the onset of diabetes mellitus. Thus, the decreased peripheral glucose disposal may not be the only mechanism of hyperglycaemia. The kinetic parameters of glucose homeostasis were evaluated in six young females aged 15, 16, 18, 19 and 24 years with generalized lipoatrophy; one patient was studied both at 12 and 15 years. Insulin resistance was evaluated in vivo by the hyperinsulinaemic euglycaemic clamp (3–4 insulin infusion rates from 1 to 100 mU/kg · min). All patients showed a rightward shift of the dose-response curve, indicating decreased insulin sensitivity. In two patients, maximal glucose disposal was moderately decreased, while in five patients it was dramatically reduced (3.6–6.9 mg/kg · min). Fasting plasma glucose was variable (4.3–18.3 mmol/l) and did not correlate with peripheral glucose disposal rates. Hepatic glucose production, measured by infusion of [6,6-2H] glucose, varied from 1.7 to 8.3 mg/kg · min and was significantly correlated with fasting plasma glucose. The overproduction of glucose despite basal hyperinsulinism suggested hepatic insulin resistance, which was confirmed by the abnormal response to constant unlabelled glucose infusion (2 mg/kg · min) in five patients. In conclusion, impaired glucose tolerance seems to develop in generalized lipoatrophy with aggravated peripheral insulin resistance. The present data show that fasting hyperglycaemia is mainly the consequence of increased hepatic glucose production.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400807
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  • 2
    Electronic Resource
    Electronic Resource
    Assessment of insulin sensitivity in glucokinase-deficient subjects (1996)
    Springer
    Diabetologia 39 (1996), S. 82-90 
    Details
    ISSN: 1432-0428
    Keywords: Insulin resistance ; glucokinase mutation ; MODY ; glucose clamp
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The chronic hyperglycaemia of glucokinase-deficient diabetes results from a glucose-sensing defect in pancreatic beta cells and abnormal hepatic glucose phosphorylation. We have evaluated the contribution of insulin resistance to this form of chronic hyperglycaemia. Insulin sensitivity, assessed by the homeostasis model assessment (HOMA) method in 35 kindreds with glucokinase mutations, was found to be significantly decreased in 125 glucokinase-deficient subjects as compared to 141 unaffected first-degree relatives. Logistic regression analysis showed that in glucokinase-deficient subjects a decrease in insulin sensitivity was associated with deterioration of the glucose tolerance status. A euglycaemic hyperin-sulinaemic clamp was performed in 14 glucokinase-deficient subjects and 12 unrelated control subjects. In six patients and six control subjects the clamp was coupled to dideutero-glucose infusion to measure glucose turnover. Average glucose infusion rates (GIR) at 1 and 5 mU · kg body weight · min−1 insulin infusion rates were significantly lower in (the glucokinase-deficient) patients than in control subjects. Although heterogeneous results were observed, in 8 out of the 14 patients GIRs throughout the experiment were lower than 1 SD below the mean of the control subjects. Hepatic glucose production at 1 mU · kg body weight−1 · min−1 insulin-infusion rate was significantly higher in patients than in control subjects. In conclusion, insulin resistance correlates with the deterioration of glucose tolerance and contributes to the hyperglycaemia of glucokinase-deficient diabetes. Taken together, our results are most consistent with insulin resistance being considered secondary to the chronic hyperglycaemia and/or hypoinsulinaemia of glucokinase-deficiency. Insulin resistance might also result from interactions between the unbalanced glucose metabolism and susceptibility gene(s) to low insulin sensitivity likely to be present in this population.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400417
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  • 3
    Electronic Resource
    Electronic Resource
    A gas chromatographic/electron impact mass spectrometric method for the isolation and derivatization of plasma taurine for use in stable isotope tracer kinetic studies (1995)
    Chichester : Wiley-Blackwell
    Biological Mass Spectrometry 30 (1995), S. 1687-1693 
    Details
    ISSN: 1076-5174
    Keywords: Chemistry ; Analytical Chemistry and Spectroscopy
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology , Physics
    Notes: To aid in the understanding of the human requirement for 2-aminoethanesulphonic acid (taurine), a method was developed for the analysis of plasma taurine and used for preliminary studies of the kinetics of plasma taurine in three healthy adult volunteers. A gas chromatographic/electron impact mass spectrometric (GC/EIMS) stable isotope ratio method was developed for the measurement of enrichment of the tracer [1,2-13C2] taurine in plasma. Natural abundance taurine and [1,2-13C2] taurine were analysed as their N-pentafluorobenzoyldi-n-butylamide (PFB-dBA) derivatives by GC/EIMS. With the addition of an internal standard, methyltaurine, the taurine concentration could also be measured. After an overnight fast, three healthy adult human subjects were given an intravenous priming dose of [1,2-13C2] taurine (3 μmol kg-1), which was immediately followed by a continuous infusion of the tracer (3 μmol kg-1 h-1) for 6 h. The mean plasma plateau enrichment was 8.07 ± 0.46 mol% excess (RSD = 5.67%) and a rate of appearance of 34 ± 2.23 μmol kg-1 h-1 was calculated. The plasma taurine concentration was found to be 56 ± 14 μmol l-1. This technique for the assessment of plasma taurine kinetics should enhance the understanding of taurine metabolism as it could be a conditionally essential amino acid in man.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jms.1190301208
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