QT dispersion in uncomplicated human obesity.

OBJECTIVE: Because obese patients generally may be prone to ventricular arrhythmias, this study was designed to measure the interval between Q- and T-waves of the electrocardiogram (QT) interval dispersion (QTD) in uncomplicated overweight and obese patients. QTD is an electrocardiographic parameter whose prolongation is thought to be predictive of the possibility of sudden death caused by ventricular arrhythmias. To better evaluate the association between obesity per se and QTD, the study population was intentionally selected because they were free of complications. RESEARCH METHODS AND PROCEDURES: QTD (defined as the difference between the maximum and the minimum QT corrected interval [QTc] across the 12-lead electrocardiogram) was measured manually in 54 obese patients (Group A: mean body mass index [BMI] of 38.1 +/- 0.9 kg/m2 [SEM], 15 males and 39 females), 35 overweight patients (Group B: mean BMI of 27.3 +/- 0.2 kg/m2, 10 males and 25 females), and 57 normal weight healthy control subjects (Group C: mean BMI of 21.9 +/- 0.2 kg/m2, 17 males and 40 females). The obese and overweight patients had no heart disease, hypertension, diabetes, or impaired glucose tolerance and did not have any hormonal, hepatic, renal or electrolyte disorders. The study subjects were matched in terms of age (mean age 38.4 +/- 1.2 years) and sex. RESULTS: The QTDs were comparable among the three groups: Group A, 56.4 +/- 2.6 ms; Group B, 56.7 +/- 2.1 ms; and Group C, 59.4 +/- 2.1 ms; not significant. The QTc intervals of Group A and Group B were similar to that of Group C (411.8 +/- 3.3, 407.2 +/- 3.9, and 410.3 +/- 3.9 ms, respectively [not significant]) and did not correlate with BMI. An association was found between QTD and QTc (r = 0.24, p < 0.005). Using multivariate stepwise regression analysis of the study population, QTD did not correlate with age, BMI, waist circumference, or abdominal sagittal diameter. DISCUSSION: These data suggest that QTD in uncomplicated obese or overweight subjects is comparable with that in age- and sex-matched normal weight healthy controls. In this study population, no association was found between QTD and anthropometric parameters reflecting body fat distribution.

Hyperinsulinemia decreases second-phase but not first-phase arginine-induced insulin release in humans.

The aim of this study was to investigate the effect of hyperinsulinemia on the first and second phase of arginine-induced insulin release in humans. Seven healthy subjects underwent three studies (lasting 360 min): a control study using saline infusion and two euglycemic clamps using a low-dose (0.33 mU.kg-1.min-1) and a high-dose (1.20 mU.kg-1.min-1) insulin infusion. After a 3-h equilibration period, arginine (25 g) was infused for 30 min, and insulin and C-peptide responses to arginine were followed for 180 min. At the end of the equilibration period, before arginine administration, steady-state insulin levels were (means +/- SE) 60.0 +/- 2.4, 165.6 +/- 1.8, and 455.4 +/- 7.8 pmol/l during saline, low-dose, and high-dose insulin infusions, respectively. The time course of insulin release during the arginine test was calculated from C-peptide concentrations by using C-peptide kinetic modeling and deconvolution. In particular, first-phase and second-phase insulin response was obtained by integrating the time course of the insulin release during either the first 5 min or the following 40 min of the arginine test, respectively. Whereas first-phase insulin release was independent of any effect induced by either insulin infusion, second-phase insulin release was reduced in a similar degree by both insulin infusion doses. First phase was 75.5 +/- 10.1, 73.7 +/- 12.8, and 73.4 +/- 10.3 pmol/kg, whereas second phase was 266.1 +/- 46.0, 143.1 +/- 33.5, and 133.0 +/- 30.2 pmol/kg for saline, low-dose, and high-dose insulin infusions, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Serum ferritin in type I diabetes.

The concentration and degree of glycosylation of serum ferritin was evaluated in type I male diabetic patients at different levels of glycaemic control. Serum ferritin did not appear to be affected by hyperglycaemia, but some patients undergoing photocoagulation had abnormally high levels of serum ferritin. The glycosylated, (concanavalin A binding), proportion of serum ferritin was essentially the same in the control and diabetic groups. The finding that hyperglycaemia does not affect the degree of enzymatic glycosylation of this serum protein is discussed.