Type 1 diabetic (T1D) patients suffer from insulinopenia and hyperglycaemia. Studies have shown that if a patient's hyperglycaemic environment is not compensated, it leads to complex immune dysfunctions. Similarly, T1D mothers with poor glycaemic control exert a negative impact on the immune responses of their newborns. However, questions concerning the impact of other metabolic disturbances on the immune system of T1D mothers (and their newborns) have been raised. To address these questions, we examined 28 T1D women in reproductive age for the relationship between various metabolic, clinical, and immune parameters. Our study revealed several unexpected correlations which are indicative of a much more complex relationship between glucose and lipid factors (namely, glycosylated haemoglobin Hb1Ac, the presence of one but not multiple chronic diabetic complications, and atherogenic indexes) and proinflammatory cytokines (IL-1alpha and TNF-alpha). Regulatory T cell counts correlated with HbA1c, diabetic neuropathy, lipid spectra parameters, and IL-6 levels. Total T-helper cell count was interconnected with BMI and glycaemia variability correlated with lipid spectra parameters, insulin dose, and vitamin D levels. These and other correlations revealed in this study provide broader insight into the association of various metabolic abnormalities with immune parameters that may impact T1D mothers or their developing child.
Acute and chronic hypoxia during the last part of pregnancy increases fetoplacental vascular resistance (Hampl & Jakoubek, Physiol Res 58: S87, 2009). Hypoxic hypoperfusion of the fetal side of the placenta is commonly considered causative in the syndrome of impaired fetal growth. Since maternal diabetes is a well‐known factor affecting fetal growth, we tested the hypothesis that maternal diabetes affects fetoplacental vascular resistance. Diabetes was induced in rats by a single injection of streptozotocin (50 mg/kg i.p.) on day 14 of pregnancy (term = 21 days). One of the placentae from each dam was prepared on day 20 and both its maternal and fetal side was perfused ex vivo with Krebs solution while fetoplacental perfusion pressure (FPPP) was measured. At constant flow rate (1 ml/min), FPPP was higher by 14% in the diabetic (D) than in the control (C) placentae (26 vs. 22 mmHg, P>0.05). Acute hypoxia increased FPPP in C (by 22%, P>0.001) and significantly less so in D (by 8%, P>0.05). During acute hypoxia FPPP did not differ between C and D. The results were similar in a different model of diabetes (100 mg/kg streptozotocin given on second postantal day to future mothers). Using this model, we also found that diabetes markedly potentiated the rise in fetoplacental vascular resistance caused by chronic hypoxia (10% O2 for the last week of pregnancy). These data indicate that experimental diabetes increases fetoplacental vascular resistance to a similar extent as acute hypoxia and potentiates the effect of chronic hypoxia.Supported by Grant Agency of the Czech Republic grant # 13‐01710S.
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