We studied glucose concentration of breast milk of nursing diabetic mothers and its possible relationship to the quality of metabolic control. Eleven Type 1 (insulin-dependent) diabetic mothers and 11 age-matched control subjects were included in the study. Although a near-normoglycemic control of diabetic mothers was accomplished by intensified insulin treatment, the HbA1 value was significantly higher in comparison to non-diabetic mothers (8.1 +/- 0.9% versus 6.2 +/- 0.5%; p less than 0.01). Regardless of this, the glucose concentration of breast milk did not differ between diabetic mothers and that of non-diabetic women (0.68 +/- 0.50 mmol/l versus 0.66 +/- 0.55 mmol/l). No correlation exists between glucose concentration of breast milk and relevant blood glucose concentration as well as glycosylated haemoglobin A1 of the mother. In conclusion, our data support the view that breast-feeding of infants of diabetic mothers is not associated with an increased offer of glucose and thus not being of importance as a possible mechanism to sustain a hyperinsulinemic state in the newborns.
Diabetic individuals frequently have platelet hyperaggregability and increased thromboxane (TXB2) production. To evaluate whether improvement of metabolic control or changes in fatty acid composition of serum lipids might alter thromboxane (TXB2) formation and platelet function, we followed up 25 newly diagnosed type 2 diabetics without angiopathy for about 6 months. Improvement of metabolic control (HbA1, fell from 12.0 +/- 0.3 to 9.0 +/- 0.3%; p less than 0.01) was associated with significant decrease in total cholesterol, triglycerides, and ratios of total cholesterol/HDL-cholesterol and LDL-cholesterol/HDL-cholesterol. Palmitic acid of phospholipids decreased significantly, whereas eicosapentaenoic acid increased. Regardless of this, the ADP-induced platelet aggregability and sensitivity were not altered. There was no effect whatever on the TXB2 synthesis capacity of clotting whole blood (204.9 +/- 25.0 vs 222.8 +/- 32.0 ng/ml) over 6 months of treatment. Platelet aggregability and TXB2 formation were not correlated to the degree of metabolic control, nor were there any correlations to serum lipids and their fatty acid composition. Thus, we are tempted to speculate that glucose metabolism in diabetes itself does not affect platelet aggregation or TXB2 formation in type 2 diabetes mellitus.
Eight type I diabetic patients received a subcutaneous injection of 10 IU regular insulin, or--after a one week interval--a suppository containing 75 IU crystalline insulin, the surfactant Brij 58, and the basic mass. In all patients there was a disease in blood glucose (onset after 20 min, maximum effect after 50 min, end of the effect after 90 min), and the plasma IRI level increased. However, the effect was attenuated in relation to the control test employing s.c. administration. The ratio of subcutaneous to rectal doses required to achieve the same effect was between 1:18 and 1:26.
For the purpose of monitoring the yield of the insulin extraction procedure from animal pancreas three methods of insulin determination were compared, i.e. the mouse convulsion test, a radioreceptor assay (RRA) on rat fat cells and a radioimmunoassay (RIA) which was especially laid out for high insulin concentrations. In samples containing actually insulin in general all three methods provided comparable results. Notable differences were only found in proinsulin-containing material. Because of its simplicity and high reproducibility as well as the good agreement of its results with those obtained with the other assays, the RIA turned out to be the most suitable assay. On the other hand, the RRA should be useful in detecting molecular differences between the investigated insulin-like preparations and standard insulin.
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