The incidence of severe hypoglycemia was determined in a 1-yr prospective study of 350 insulin-dependent diabetic (IDDM) children. There were no significant differences in mean glycosylated hemoglobin, age, and duration of disease between the patients who had severe hypoglycemia and those who did not. There were 25 episodes in 24 patients (6.8%). Their insulin doses at the time of the episode (U.kg-1.day-1) were significantly higher than those of the nonhypoglycemic group (mean +/- SD 1.01 +/- 0.30 vs. 0.89 +/- 0.29; P = .04). The hypoglycemic group had a significantly higher mean number of previous episodes of severe hypoglycemia than the nonhypoglycemic group (0.92 +/- 1.18 vs. 0.25 +/- 0.68; P = .01). In only 64% of the episodes, an unusual circumstance such as strenuous physical activity or missed or delayed meals preceded the event. Multivariate analysis of the data by logistic regression showed risks of developing hypoglycemia of 2.5 per 0.5 U/day insulin and of 2.0 per previous episode of severe hypoglycemia. We conclude that severe hypoglycemia may be a recurrent problem in some diabetic children, but it does not appear to be related to age or blood glucose control. The presence of previous episodes may be a guide to identify patients at greater risk of developing severe hypoglycemia. Adherence to regular testing, strict spacing and consistency of meals, and extra food for extra activity may reduce this serious complication.

Three hundred twelve diabetic children and adolescents were seen in our diabetic clinic and instructed to test their capillary blood glucose (CBG) twice daily and to use an algorithm to adjust their short-acting insulin. Of this group, 219 youngsters had a full 3-yr period of observation. At each clinic visit, blood was obtained for fasting blood glucose and HbA1 and, once a year, cholesterol and triglycerides were also measured. Patient and parent accuracy in measuring CBG was found to be adequate. The changes over time in HbA1 were nondifferential across age and sex, and there was no difference in the level of HbA1 between age and sex groups, the number of tests reported to have been done by the patients, the number of injections of insulin per day, or the serum cholesterol. There was a significant relationship between the HbA1 and the fasting blood glucose (P less than .001) measured by the laboratory as well as with the serum triglyceride (P less than .01). The failure to improve diabetic control, despite measures that would have been expected to do so, was believed to relate more to a lack of compliance than to a flaw in the therapeutic approach. It was interesting to note that the adolescent patients in the study were in no worse control than the younger children in the group. Although better technical skills are available today to manage diabetes, the psychosocial approach to patient motivation requires improvement.

Examining the relationship of stress, dietary disinhibition, and blood glucose control in diabetic young women was the goal of this study. Sixty-five diabetic girls and women, ranging in age from 12 to 26 years, completed eating behaviors and perceived stress scales during regular clinic visits. Blood glucose control was assessed by concurrent glycosylated hemoglobin measurements. Multiple regression analyses indicated that high levels of perceived stress predicted dietary disinhibition and that within the age range studied, young women were more likely than early adolescent girls to perceive their life as stressful. Contrary to previous findings that failed to show that stress can indirectly affect glucose control by interfering with compliance behaviors, the present work indicated a Stress X Dietary Disinhibition interaction in predicting glucose control. Blood glucose control was poorest in those diabetic women who both perceived their lives as stressful and reported medium to high disinhibition. Blood glucose control was unrelated to stress in young women who reported low levels of disinhibition. These results have implications for the development of specific interventions for young diabetic women who perceive their lives as stressful and who may respond to stress by eating.

We have studied the effects of a cardiac sparing thyromimetic, CGS 23425, on postprandial levels of triglycerides, abundance of apolipoprotein B (apo B) protein and hepatic apo B mRNA expression in rats. When compared with control rats, triglyceride clearance was significantly accelerated by treatment with CGS 23425. A full return to baseline values was achieved within 8 h after ingesting a large quantity of fat, as compared to >24 h in control animals. The abundance of apo B-100 protein in CGS 23425-treated hyperlipidemic rats decreased in a dose-dependent manner, but levels of apo B-48 were not significantly affected. Like -triiodothyronine (-T 3 ), treatment with 30 µg/kg CGS 23425 for 6 or 9 days decreased the levels of apo B-100 protein by 80% and 40% respectively. This change was paralleled by a 27% reduction in hepatic apo B-100 mRNA. To investigate a potential mechanism of CGS 23425 action, we measured in vitro apo B mRNA editing activity in hepatocellular extract from control or CGS 23425-treated rats. Treatment with CGS 23425 increased activity of the hepatic apo B-100 editosome, apobec-1. In human hepatoma cells which lack apobec-1 activity, apo B-100 mRNA levels remained the same in cells treated with or without the agent. In summary, these observations show that CGS 23425 decreases the levels of apo B-100 in rats. This action of CGS 23425 involves apo B-100 mRNA editing activity.