These data (the only data so far available in Caucasians) support the viewpoint that for the identification of people at high risk of diabetes, the use of the OGTT should be maintained.

No abstract

that the lesion may be the result of a hitherto unknown type of hypersensitivity response.Our results do not show that the adverse effects of practolol are due to a hypersensitivity reaction, but two pieces of evidence might tentatively support such a conclusion. The first is the low antibody concentrations found in the sera of patients with sclerosing peritonitis. This might have been due to a reduction in antigenic stimuli, since the patients had been taken off the drug some time before the clinical signs of intestinal obstruction appeared. Equally, however, the results could be explained by postulating that the antigenic metabolite is incorporated into connective tissue and the mass of antigenic determinants presented by the peritoneum is sufficient to fix most of the circulating antibody. The second piece of evidence is perhaps more pertinent and concerns the challenge study on one of the patients (case 4). This patient had high concentrations of circulating antibody before challenge with practolol, and when the drug was given, clinical signs of the tissue damage were produced. Other patients in the study might have shown an adverse response if the drug had been given for a longer period.Continued analysis of serum will probably provide only circumstantial evidence of a practolol-induced hypersensitivity reaction. An animal model is needed to study the tissue damage produced by the drug, and we are currently engaged in studies of this kind.

Eight type II (non-insulin-dependent) normolipidemic diabetic patients (aged 45 +/- 15 yr, body mass index 22 +/- 2 kg/m2, means +/- SD) treated with diet alone or diet plus oral hypoglycemic agents were given, in random order for periods of 15 days, two diets with different carbohydrate (CHO) (40 vs. 60% of total calories) and fat (20 vs. 40%) levels. Simple CHO, fiber, saturated fat, cholesterol, and polyunsaturated-saturated fat ratio were similar in the two diets. Total plasma cholesterol was not significantly affected by dietary changes; conversely, plasma triglyceride (1.38 +/- 0.59 vs. 1.11 +/- 0.39 mM, P less than 0.05) and apolipoprotein CII (3.8 +/- 1.4 vs. 3.3 +/- 0.8 mg/dl) increased significantly after the high-CHO low-fat diet. Among the various lipoproteins, very-low-density lipoprotein (VLDL) was the most affected by diet: VLDL cholesterol concentrations increased from 0.30 +/- 0.19 to 0.43 +/- 0.28 mM (P less than 0.05), and triglyceride concentrations increased from 0.62 +/- 0.33 to 0.88 +/- 0.53 mM (P less than 0.05). In conclusion, increasing the amount of complex CHO in the diet induces an elevation of VLDL in normolipidemic, nonobese, mildly type II diabetic patients.