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.

Summary. Forty-four children with Type 1 (insulin-dependent) diabetes (aged 0.7-16.7 years) were observed from diagnosis for cytoplasmic islet cell antibodies and serum C-peptide concentrations. Islet cell antibodies were analysed by indirect immunofluorescence for both conventional IgG and complement-fixing antibodies. Thirty-seven children (84%) were found to be positive for conventional islet cell antibodies at diagnosis, and 21 (48%) remained positive over the observation period. Twenty-six patients (59%) were positive for complement-fixing antibodies at diagnosis and eight remained so during the follow-up period. The serum C-peptide concentrations increased significantly during the first 3 months after diagnosis, after which there was a gradual decrease in the levels. Those children who remained positive for complement-fixing antibodies over the observation period had significantly higher serum C-peptide concentrations on several occasions during the second year and had also a higher integrated serum C-peptide concentration over the initial 2 years than those who became negative for complement-fixing antibodies. These observations suggest that the continuous production of complement-fixing islet cell antibodies in those patients who are positive for these antibodies at diagnosis presupposes the preservation of a sufficient amount of functioning/~ cells for antigenic stimulation. These results support the view that the complement-fixing islet cell antibodies reflect ongoing destructive processes in the/3 cells.

The urinary excretion excretion of albumin and Beta2-microglobulin was measured by radioimmunoassay in 64 children and adolescents with Type 1 (insulin dependent) diabetes and in 68 non-diabetic subjects aged from 9 to 19 years. At rest the albumin excretion of te diabetic subjects did not differ from that of te non-diabetic children and adolescents but during exercise the albumin excretion was significantly higher in children and adolescents with Type 1 diabetes (p less than 0.02). the excretion rate of Beta2-microglobulin in diabetic subjects did not differ from that of the healthy subjects. Both at rest and during exercise the albumin excretion rate was highest in those diabetics with poorest metabolic control of their disease.

Abstract. Clinical and autoimmune characteristics of 150 diabetic children of mean age 7.8 years (SD 4.1 years) were recorded at clinical manifestation and during the first 2 years of IDDM in order to investigate whether subjects with high risk HLA-DQB1 genotypes differ from those without these risk markers. When comparing subjects with the DQB1*0302/0201, DQB1*0302/x, DQB1*0201/x, or other DQBl genotypes (x = no protective allele), no differences were found in the age of the subjects at diagnosis, the duration of hyperglycaemic symptoms, or the length of clinical remission. The frequency of islet cell antibodies (ICA) and quantitative serum levels of these antibodies were of the same magnitude in all four groups. During the initial 2 years of IDDM serum C-peptide concentrations were observed to be inversely related to the degree of genetic risk ( P < 0.001 in two-way analysis of variance for repeated measures), the lowest C-peptide levels being observed in the group of DQBl*O302/0201 heterozygotes ( P < 0.001 vs. DQB1*0201/x; P < 0.01 vs. DQB1*0302/x; P = 0.05 vs. others). On the other hand, the subjects with the DQB1*0201 genotype had the highest serum C-peptide concentrations, the levels being even higher than those of the patients carrying neutral or protective DQB 1 genotypes ( P < 0.01). These subjects also had lower daily insulin doses and blood glycated haemoglobin A, (HbA,) levels over the initial 2 years of the disease when compared with the DQB 1 *0302/0201 heterozygotes (P < 0.05 and P < 0.01, respectively). We conclude that the DQB 1 *0302/020 1 heterozygous individuals with the greatest genetic risk of IDDM lack the capacity for recovery of @-cell function commonly seen in other subjects after starting exogenous insulin treatment. Our results also suggest that the 106 DQB1*0201/x genotype is associated with a milder form of the disease, since these subjects were characterized by a transient recovery of @-cell function accompanied by lower requirement of exogenous insulin and better metabolic control over the initial 2 years of IDDM.