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Hyperglycaemic Conditions (hyperglycaemic + condition)
Selected AbstractsInfluence of Hyperglycaemia on Chemical-Induced Toxicity: Study with Cyclophosphamide in RatBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 4 2009Kalavatala Saandeep Hyperglycaemia perturbs the critical balance between oxidative stress and anti-oxidant defence mechanisms in the body and thereby alters the response of biological system towards various toxic chemicals. Cyclophosphamide (CP) is a widely prescribed anticancer drug, well-known genotoxic agent as well as used in the development of immunocompromised animal models. The present study investigated the modulating effect of diabetes on the cyclophosphamide-induced cytotoxicity and genotoxicity. The study was performed on male Sprague-Dawley rats (200 ± 10 g). Cyclophosphamide (10 mg/kg) was administered five consecutive days in a week for 3 weeks to both control and diabetic rats. Thiobarbituric acid reactive substances (TBARS) levels were measured in the plasma, liver, kidney and lung tissues. DNA damaging potential of cyclophosphamide under diabetic condition was evaluated using comet and halo assay as an endpoint. To further ascertain the mode of cell death, terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) assay and immunohistochemical evaluation of p53 was performed. Significant increase in DNA damage was revealed by the comet assay parameters, halo assay indicated the level of cytotoxicity and the oxidative stress was measured using the TBARS assay in the diabetic rats receiving cyclophosphamide treatment. The toxic effects were more prominent in diabetic animals as compared to non-diabetic rats. Cyclophosphamide treatment and diabetic condition per se led to increase in the p53 + and TUNEL + cells in the liver and kidney of rats. Under diabetic condition, further increase in the p53 + and TUNEL + cells was observed in response to cyclophosphamide. In the present study, we report that hyperglycaemic condition exaggerates the cyclophosphamide-induced toxicity and the response was found to be tissue specific. [source] Exercise-induced growth hormone response in euglycaemia and hyperglycaemia in patients with Type 1 diabetes mellitusDIABETIC MEDICINE, Issue 2 2010S. Jenni Diabet. Med. 27, 230,233 (2010) Abstract Aims, To compare exercise-induced growth hormone (GH) response in patients with Type 1 diabetes during stable euglycaemic and hyperglycaemic conditions. Methods, We conducted a randomized, controlled, single-blinded cross-over trial in seven male patients with well-controlled Type 1 diabetes. The patients cycled twice for 120 min at a level of 55,60% maximal oxygen uptake. Euglycaemia was at 5.0 mmol/l, hyperglycaemia at 11.0 mmol/l. Results, Area under the curve of GH (AUCGH) during exercise was significantly higher during euglycaemia [1430 ng ml,1 min, 95% confidence interval (CI) 703,2910] compared with hyperglycaemia (1061 ng ml,1 min, 95% CI 538,2091, P = 0.02). Conclusions, In patients with Type 1 diabetes, GH concentrations during moderate aerobic exercise during stable hyperglycaemic conditions are significantly lower compared with euglycaemia. These findings are compatible with preserved glucose-mediated GH regulation during exercise in individuals with well-controlled Type 1 diabetes. [source] Effect of acute hyperglycaemia on sensory processing in diabetic autonomic neuropathyEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2010Jens B. Frøkjær Eur J Clin Invest 2010; 40 (10): 883,886 Abstract Background, Acute hyperglycaemia is known to increase gastrointestinal (GI) sensitivity in healthy subjects and may contribute to the increased prevalence of GI symptoms in diabetes patients. The aim of this study was to evaluate the effect of acute hyperglycaemia on perception and brain responses to painful visceral and somatic stimuli in diabetic patients. Materials and methods, The sensitivity and evoked brain potentials (EPs) to electrical oesophageal and median nerve stimulations were assessed in 14 type-1 diabetes patients with autonomic neuropathy and GI symptoms using a hyperinsulinaemic clamp at 6 and 15 mM. Results, No differences between the normo- and hyperglycaemic conditions were found in sensitivity to both oesophageal (P = 0·72) and median nerve (P = 0·66) stimulations. The latencies and amplitudes of EPs did not differ between the normo- and hyperglycaemic conditions following oesophageal (P = 0·53 and 0·57) and median nerve (P = 0·78 and 0·52) stimulations. Conclusions, Acute hyperglycaemia itself does not contribute to the sensations in patients with longstanding diabetes and autonomic neuropathy. Any potential sensory effects of acute hyperglycaemia can likely be blurred by the neuropathic-like changes in the sensory nervous system. [source] |