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Nocturnal hypoglycaemia may contribute to sudden death in diabetic patients. However, it is not well known why hypoglycaemia makes these patients prone to death. We assessed the effects of controlled hypoglycaemia on cardiac repolarisation using novel electrocardiographic descriptors of T-wave and QRS complex morphology in 16 type 1 diabetic patients and eight healthy counterparts. Several electrocardiographic variables characterising repolarisation were analysed from digitised 12-lead electrocardiograms during a euglycaemic and a hypoglycaemic clamp. Hypoglycaemia did not result in significant changes either in the QT interval corrected for heart rate by the nomogram method or in QT dispersion. However, the morphology of the T-wave changed significantly during hypoglycaemia. The T-wave amplitude and area in precordial leads decreased significantly in both groups (p

Aims/hypothesis. Inflammation could play a part in insulin resistance. Thiazolidinediones, new antidiabetic drugs, possess anti-inflammatory effects in vitro. We investigated if acute-phase serum proteins are increased in patients with Type II (non-insulindependent) diabetes mellitus who had been treated with insulin and whether troglitazone has anti-inflammatory effects in vivo. Methods. A total of 27 patients (age 63.0 ‐ 1.7 years, HbA 1c 8.8 ‐ 0.3 %, BMI 32.7 ‐ 0.8 kg/m 2 , duration 15.2 ‐ 1.4 years, insulin dose 73.3 ‐ 7.0 U/day) participated in the study. The patients received daily either 400 mg troglitazone or placebo for 16 weeks. Blood samples were taken at baseline, at the end of therapy and after a follow-up time of 23 ‐ 4 days. Results. The concentrations of serum amyloid A (6.2 ‐ 1.1 mg/l) and C-reactive protein (6.1 ‐ 1.1 mg/ l) were increased (p < 0.001) and complement protein C3 (1.69 ‐ 0.05 g/l) was also above the reference range for healthy subjects. Placebo treatment had no effect on glucose or inflammation, whereas troglitazone reduced fasting glucose (from 10.4 ‐ 0.6 mmol/l to 8.1 ‐ 0.5 mmol/l, p < 0.01), HbA 1c (from 8.7 ‐ 0.3 % to 7.5 ‐ 0.3 %, p < 0.01), insulin requirements (from 75 ‐ 10 U/day to 63 ‐ 10 U/day, p < 0.05), serum amyloid A (from 6.3 ‐ 1.5 mg/l to 4.0 ‐ 1.3 mg/l, p = 0.001), a-1-acid glycoprotein (from 906 ‐ 51 mg/l to 729 ‐ 52 mg/l, p = 0.001) and C3 (from 1.72 ‐ 0.07 g/l to 1.66 ‐ 0.06 g/l, p < 0.05) but not a-1-antitrypsin, ceruloplasmin, C-reactive protein or haptoglobin significantly. Concentrations of glucose and acute-phase reactants had returned to those before treatment at the follow-up visit. Conclusion/interpretation. In Type II diabetic patients serum amyloid A and complement protein C3 are raised. Troglitazone exerts a selective reversible action on some acute-phase proteins and C3 but not on others in conjunction with the improvement in glucose metabolism. [Diabetologia (1999) 42: 1433‐ 1438]