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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 9 (1973), S. 461-466 
    ISSN: 1432-0428
    Keywords: Erythrocyte 2.3-DPG ; diabetes ; blood glucose variation ; islet cell tumor ; insulin ; tolbutamide ; microangiopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary No significant differences were found in the erythrocyte 2.3-DPG concentration between 14 normals (16.82±0.66 μmoles 2.3-DPG/g Hb) and 44 diabetic patients (16.22±0.38 μmoles 2.3-DPG/g Hb). However, in diabetic patients we could demonstrate significant fluctuations determined by the metabolic control of their diabetes. Hyperglycaemic patients (n = 10) developed during treatment, concomitant with declining blood glucose, a significant decrease to 13.97± 0.64 [mioles 2.3-DPG/g Hb. After normalization of blood glucose the 2.3-DPG level rose again. Two patients with islet cell tumors had a fluctuation in the 2.3-DPG concentration of about 20%, when symptomatic hypoglycaemia occurred during an extended fast. This variation in 2.3-DPG dependent upon changes in blood glucose was also demonstrated in-vitro by a dialysis technique where glucose was kept constant at 400 or 80 mg/100 ml. Incubating hyperglycaemic blood (n = 6) of uncontrolled diabetics in a high glucose medium, 2.3-DPG was constant over 7 h, whereas at low glucose concentration 2.3-DPG dropped significantly (p 〈 0.001). Blood from nondiabetic subjects did not show this phenomenon. In-vitro additions of insulin and tolbutamide failed to produce an effect on 2.3-DPG. Our results suggest that pronounced fluctuations of blood glucose in diabetics influence 2.3-DPG levels in erythrocytes and thus might impair peripheral oxygen supply.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Blutlaktat ; Buformin ; Diabetes ; Dichlorazetat ; Blood lactate ; buformin ; diabetes ; dichloroacetate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary In animals, dichloroacetate (DCA) which activates pyruvate dehydrogenase has been shown to diminish increased blood lactate concentrations due to biguanide treatment. In 10 maturity onset diabetics, therefore, the effect of a combined therapy with buformin and DCA (200 mg b.i.d.) was studied on blood lactate concentrations and compared with an analogous pre- and postinvestigation period of 6 days with buformin treatment alone (100 mg b.i.d.). Mean blood glucose concentrations remained the same during all 3 investigation periods. Also, neither fasting nor postprandially significant differences were found in blood lactate and ketones. In association with a standardized ergometer test, however, the rise in blood lactate was significantly smaller (p〈0.05) while the patients were on buformin plus DCA, compared to the periods when only buformin was given. Furthermore, less ketone bodies appeared to be utilized by the exercising muscle under the influence of the combined treatment (p〈0.05). These results are in good agreement with animal studies and suggest that DCA might be as effective in decreasing enhanced blood lactate concentrations in biguanide treated man as in animals.
    Notes: Zusammenfassung Im Tierversuch vermag Dichlorazetat (DCA), das die Pyruvatdehydrogenase stimuliert, erhöhte Blutlaktatspiegel unter Biguaniden zu senken. Bei 10 Erwachsenendiabetikern wurde daher der Einfluß einer Kombinationsbehandlung mit Buformin und DCA (400 mg tgl.) auf die Blutlaktatspiegel untersucht und mit einer analogen Vor- und Nachperiode einer alleinigen Buforminbehandlung (200 mg tgl.) über 6 Tage verglichen. Die Diabeteseinstellung blieb gemessen an den mittleren Blutglucosekonzentrationen während der 3 Untersuchungsperioden unverändert. Ebenfalls keine signifikanten Unterschiede, weder nüchtern noch postprandial, ergaben sich hinsichtlich der Laktat-und Ketonkörperspiegel im Blut. Im Anschluß an einen standardisierten Ergometertest jedoch stieg unter der Kombinationstherapie mit Buformin und DCA das Blutlaktat wesentlich geringer an (p〈0,05) als unter Buformin allein. Gleichzeitig wurden unter der Kombinationstherapie weniger Ketonkörper vom arbeitenden Muskel utilisiert (p〈0,05). Diese Ergebnisse stimmen mit Tierversuchen gut überein und können im Sinne einer vermehrten Pyruvatoxidation unter DCA interpretiert werden; es ist zu hoffen, daß DCA ähnlich wie beim Tier auch bei biguanidbehandelten Diabetikern einem excessiven Ansteigen der Blutlaktatspiegel vorbeugen kann.
    Type of Medium: Electronic Resource
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