We wanted to determine the levels of fasting serum insulin during growth, the tracking of serum insulin, and the correlation of serum insulin with other coronary heart disease risk indicators in children and young adults. In 1986 2433 subjects, aged nine to 24 were studied, and insulin data were available from the same population in 1980 and 1983. Serum insulin levels showed a peak during puberty in both sexes and the decline in insulin continued after the age of 21. Tracking of serum insulin was only moderate, especially in females and young boys. Serum insulin correlated positively with body mass index, concentrations of serum triglycerides, and blood pressure, and inversely with the concentration of high density lipoprotein cholesterol. High triglycerides, high systolic blood pressure, and low level of high density lipoprotein cholesterol clustered among subjects within the highest insulin quartile. Our results suggest that the insulin resistance phenomenon, caused mainly by obesity and leading to unfavourable levels of other coronary heart disease risk indicators, is already developing in children and young adults. This suggests that preventing obesity in early life is important.

To examine whether a physical activity program could improve physical fitness and glycemic control, 32 children and adolescents with insulin-dependent diabetes mellitus (IDDM) were examined before the program and 3 mo later. Fifty percent of the subjects (n = 16) participated in the training for 1 h/wk (exercise group), whereas the remaining subjects were engaged in nonphysical activities for an equal amount of time (nonexercise group). Age of the subjects ranged from 8.2 to 16.9 yr, (mean 11.9 yr), with mean duration of diabetes 0.6-13.1 yr (5.2 yr). During the 3-mo program peak oxygen consumption (VO2) rose from 40.0 to 43.8 ml.min-1.m-2 (P less than .01) in the exercise group but only by 1.3 ml.min-1.m-2 in the nonexercise group (NS). Metabolic control did not improve in either group, with glycosylated hemoglobin level rising from 9.8 to 10.5% (P less than .01) in the exercise group and from 9.4 to 9.7% (NS) in the control group. When subjects were stratified according to their participation, metabolic control was significantly better among diabetic subjects participating frequently (greater than or equal to 11 of 13 sessions) than among those participating infrequently (less than 11 of 13 sessions), regardless of the type of activity. It was concluded that a training program of 1 h/wk for 3 mo does improve physical fitness but not the metabolic control of diabetes. On the other hand, glycemic control appears to be best among diabetic subjects who are motivated to participate in any kind of program related to the treatment of their disease.

To evaluate the efficacy of different antipyretic agents and their highest recommended doses for preventing febrile seizures. Design: Randomized, placebo-controlled, doubleblind trial. Setting: Five hospitals, each working as the only pediatric hospital in its region.

The effects of synthetic GHRH-(1-44) (1 microgram/kg, iv), clonidine (0.15 mg/m2, orally), L-dopa (0.5 g, orally), and insulin (0.1 IU/kg, iv) on plasma immunoreactive (ir) GHRH and GH levels were determined in normal men, aged 31-46 yr (n = 4-8). In addition, plasma ir-GHRH and GH concentrations were determined before and after the administration of clonidine in six younger men, aged 19-25 yr. GHRH was extracted from plasma using Sep-Pak C18 cartridges and measured with a mid-portion-specific GHRH antiserum. The mean plasma ir-GHRH and GH levels ranged from 9-11 ng/L and 0.5-1.5 microgram/L, respectively, in the older men during a 2-h control study. After GHRH administration, the mean plasma ir-GHRH concentration increased to a peak of 512.5 ng/L at 3 min and GH to a peak of 9.2 micrograms/L at 10 min. Clonidine resulted in a significant increase in mean plasma GH levels (P less than 0.05) in the younger men, but not in the older men. Plasma ir-GHRH concentrations did not change after clonidine. L-Dopa increased plasma ir-GHRH at 60 min (P less than 0.05) and GH at 60-120 min (P less than 0.05). Insulin-induced hypoglycemia increased plasma GH levels (to a mean of 23.8 micrograms/L at 60 min; P less than 0.001), whereas plasma ir-GHRH levels did not change. We conclude that the mechanisms of the various GH stimulation tests differ. Some GH responses, including those induced by insulin, do not appear to be mediated by GHRH.