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  • Articles: DFG German National Licenses  (5)
  • diabetes  (3)
  • insulin-dependent diabetes mellitus  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 37 (1994), S. 1132-1141 
    ISSN: 1432-0428
    Keywords: Lymphocyte subsets ; insulin-dependent diabetes mellitus ; gestational diabetes ; cord blood
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate the impact of diabetic mothers on the maturation of the immune system in their offspring, immunophenotypic markers of major lymphocyte subpopulations were evaluated by two-colour flow cytometric analysis in 160 healthy children of diabetic mothers (100 with insulin-dependent diabetes mellitus (IDDM); 48 with gestational diabetes), including 22 neonates, 45 infants aged 8–12 months, 46 children aged 1–2 years, 29 children aged 3–6 years and 18 children aged 7–17 years. Results were compared with 21 neonates of healthy mothers from our hospital and with 110 paediatric subjects of a reference population. In neonates of diabetic mothers, percentages of total lymphocytes (p=0.044), T and B lymphocytes (p=0.004, respectively) were significantly decreased compared to our neonates of healthy mothers. By subdividing the group of neonates in offspring of mothers with IDDM (n=15) or gestational diabetes (n=7), differences compared to normal neonates were mainly observed in neonates of mothers with IDDM (T lymphocytes: p=0.006; B lymphocytes: p=0.008). In cord blood, 45.5% of neonates had antibodies to islet cells, insulin or glutamic acid decarboxylase, most likely transmitted through the placenta of the diabetic mother. No association was found between alterations of lymphocyte subsets and antibody-positivity in cord blood, nor was there any correlation of lymphocyte counts and mean HbA1 during pregnancy, maternal age at delivery, diabetes duration, or neonatal birth weight, respectively. Comparisons among age groups from newborn infants through adolescents revealed higher percentages of total lymphocytes and lower percentages of activated T cells in children of diabetic mothers compared to children of the reference population between the age of 1 to 6 years (67–73% of the cases above and 62–77% below the interquartiles of the reference range, respectively). No significant differences in lymphocyte subpopulations between children of mothers with IDDM diabetes and gestational diabetes have been detected. In addition, there were no abnormalities of lymphocyte subsets in children who are at high risk for the development of IDDM. In summary, we suggest that the observed changes in children of diabetic mothers may reflect a cellular immune reaction to the particular maternal environment, characterized by both an abnormal metabolic state and persisting autoimmunity in the affected mother.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 37 (1994), S. 1132-1141 
    ISSN: 1432-0428
    Keywords: Key words Lymphocyte subsets ; insulin-dependent diabetes mellitus ; gestational diabetes ; cord blood.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate the impact of diabetic mothers on the maturation of the immune system in their offspring, immunophenotypic markers of major lymphocyte subpopulations were evaluated by two-colour flow cytometric analysis in 160 healthy children of diabetic mothers (100 with insulin-dependent diabetes mellitus (IDDM); 48 with gestational diabetes), including 22 neonates, 45 infants aged 8–12 months, 46 children aged 1–2 years, 29 children aged 3–6 years and 18 children aged 7–17 years. Results were compared with 21 neonates of healthy mothers from our hospital and with 110 paediatric subjects of a reference population. In neonates of diabetic mothers, percentages of total lymphocytes (p = 0.044), T and B lymphocytes (p = 0.004, respectively) were significantly decreased compared to our neonates of healthy mothers. By subdividing the group of neonates in offspring of mothers with IDDM (n = 15) or gestational diabetes (n = 7), differences compared to normal neonates were mainly observed in neonates of mothers with IDDM (T lymphocytes: p = 0.006; B lymphocytes: p = 0.008). In cord blood, 45.5 % of neonates had antibodies to islet cells, insulin or glutamic acid decarboxylase, most likely transmitted through the placenta of the diabetic mother. No association was found between alterations of lymphocyte subsets and antibody-positivity in cord blood, nor was there any correlation of lymphocyte counts and mean HbA1 during pregnancy, maternal age at delivery, diabetes duration, or neonatal birth weight, respectively. Comparisons among age groups from newborn infants through adolescents revealed higher percentages of total lymphocytes and lower percentages of activated T cells in children of diabetic mothers compared to children of the reference population between the age of 1 to 6 years (67–73 % of the cases above and 62–77 % below the interquartiles of the reference range, respectively). No significant differences in lymphocyte subpopulations between children of mothers with IDDM diabetes and gestational diabetes have been detected. In addition, there were no abnormalities of lymphocyte subsets in children who are at high risk for the development of IDDM. In summary, we suggest that the observed changes in children of diabetic mothers may reflect a cellular immune reaction to the particular maternal environment, characterized by both an abnormal metabolic state and persisting autoimmunity in the affected mother. [Diabetologia (1994) 37: 1132–1141]
    Type of Medium: Electronic Resource
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  • 3
    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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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 11 (1975), S. 255-260 
    ISSN: 1432-0428
    Keywords: Bohr effect ; diabetes ; erythrocyte 2,3-DPG ; Hill-coefficient ; ketoacidosis ; oxygen affinity of whole blood ; P50 act pH ; plasma inorganic phosphate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Daily evaluations of 8 newly detected ketoacidotic diabetics showed the Bohr-effect of haemoglobin to be decreased by 50% while erythrocyte 2,3-DPG was decreased below 10 μmoles/g Hb. 2,3-DPG correlated strongly with pH during acidosis and with plasma inorganic phosphate (Pi) subsequently to the first insulin administration. Oxygen affinity of haemoglobin, measured as P50 act pH, was unchanged in ketoacidosis compared to the time before discharge. After correction of acidosis, however, P50 act pH fell strikingly (p 〈 0.001) and remained decreased up to 7 days depending upon the resynthesis of 2,3-DPG in relation to Pi. The Hill-coefficient n reflecting the slope of the oxygen dissociation curve was diminished in ketoacidosis (p 〈 0.005), and decreased further after pH-normalization (p 〈 0.005). There was a close association of n with 2,3-DPG (p 〈 0.001) and additionally with Pi at 2,3-DPG-levels below 10 μmoles/ g Hb. Based on these findings a decreased erythrocyte oxygen release of one fifth during acidosis and more than one third after pH-correction can be hypothesised. In view of the intimate relation of Pi to the oxygen transport system it is suggested that treatment of ketoacidosis should include Pisubstitution.
    Type of Medium: Electronic Resource
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  • 5
    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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