OBJECTIVE -The aim of this study was to measure forearm blood flow (FBF) to detect any possible changes that might indicate vascular disorders in children and adolescents with type 1 diabetes.RESEARCH DESIGN AND METHODS -FBF was measured by near-infrared spectroscopy (NIRS), venous occlusion at rest, and after handgrip exercise. A total of 40 children and adolescents with type 1 diabetes and 40 healthy children and adolescents (6 -18 years) were matched for age and sex for comparison.RESULTS -In the diabetic group (age 12.79 Ϯ 2.9 years, duration of diabetes 51.5 Ϯ 36 months), FBF at rest was significantly lower (1.39 Ϯ 0.76 ml ⅐ 100 g muscle -1 ⅐ min -1 ) than in control subjects (age 12.66 Ϯ 2.9 years, FBF at rest 1.90 Ϯ 1.19 ml ⅐ 100 g muscle -1 ⅐ min -1 ). After exercise, FBF increased significantly less in the diabetic group (0.70 Ϯ 0.82 ml ⅐ 100 g muscle -1 ⅐ min -1 ) compared with the control subjects (1.15 Ϯ 1.05 ml ⅐ 100 g muscle -1 ⅐ min -1 ). FBF at rest decreased with increasing age in both groups. The change in FBF after exercise was independent of age in the diabetic group and increased with increasing age in control subjects. FBF is reduced with impaired hyperemic response after exercise in children and adolescents with type 1 diabetes.CONCLUSIONS -These data suggest that vascular disorders in childhood are detectable noninvasively by NIRS. Diabetes Care 27:1942-1946, 2004D iabetes is one major risk factor for development of vascular disorders. Vascular disorders described in childhood are microvascular complications of the eye, kidney disorders (low creatinine clearance, fluctuating microproteinuria), or echocardiographic changes (1-4).With near-infrared spectroscopy (NIRS), a relatively new technique, an assessment of skeletal muscle blood flow, especially of the small vessels, is possible and has been validated in several studies (5-9). By means of NIRS, impaired peripheral muscle blood flow and oxygenation has been detected in adult patients with diabetes, peripheral vascular disease, and heart failure (10 -12).No data on muscle blood flow in children and adolescents with type 1 diabetes have been published until now. In the present study, skeletal muscle forearm blood flow (FBF) was measured by means of NIRS in children and adolescents with type 1 diabetes without otherwise clinically detectable microangiopathy and in healthy control subjects. The aim of the present study was to investigate whether muscle blood flow measured by NIRS is already impaired in children and adolescents with type 1 diabetes in the absence of any other clinical signs of vasculopathy. RESEARCH DESIGN ANDMETHODS -Children and adolescents with type 1 diabetes aged 6 -18 years were studied. Patients with microalbuminuria and eye diseases were excluded from the study. Furthermore, patients had to have no evidence of neuropathy, cardiac failure, or intermittent claudication. Both patients with type 1 diabetes and control subjects who were obese or had taken any medication (except insulin) within the last 7 days were exclud...

Serum leptin levels were positively correlated with adiposity in obese children and a diet and sports intervention program decreased serum leptin, insulin and body fat in all children. Changes in leptin were best described by the initial leptin concentration. The increase in correlation of leptin with %FM in obese pubertal boys after the intervention could have its underlying mechanism in an increased sensitivity to leptin and anabolic hormones.

Recent findings have questioned the independent influence of insulin on leptin. We studied whether insulin contributes to leptin in obese children, independent of confounding parameters, such as total adiposity, fasting insulin resistance index, and fat free mass. In 100 obese boys and 103 obese girls, blood levels of leptin, insulin, glucose, and triglycerides were determined. The fasting insulin resistance index (FIRI) was calculated, and body composition was assessed by means of impedance. Leptin and glucose were higher in girls, and all estimates of adiposity were significantly associated with leptin. However, when adjusted for adiposity, the relationship between insulin and leptin, and also between FIRI and leptin, remained significant in boys and girls (p<0.05). Although several regression models were tested, neither insulin nor FIRI were found to contribute significantly and independently to leptin. BMI together with triglycerides and FFM were the main determinants for the variation in leptin in boys (adj. R2=0.46, p<0.0001). In girls, BMI explained a great magnitude of the variation in leptin (adj. R2=0.60, p<0.0001). These findings indicate that in the state of childhood and adolescent obesity, total adiposity but not insulin or insulin resistance index is the main determinant for leptin. In contrast to obese girls, the fat free mass and triglycerides contribute significantly to the variation in leptin in obese boys. The biological significance for these findings should be elucidated in longitudinal studies.

This study shows that ghrelin might not regulate the GH response to insulin-induced hypoglycaemia in prepubertal and pubertal children. A role for ghrelin in the regulation of cortisol secretion can be hypothesized concerning the negative correlation between changes in ghrelin and cortisol. Furthermore, the results imply that ghrelin secretion is age dependent and is a function of growth.

This study addresses whether the expected relationship of 15 specified subcutaneous adipose tissue layers (SAT layers) from 1-neck to 15-calf and body fat mass (FM) with leptin was influenced by a weight-loss program. In 30 obese girls (10 prepubertal, 15 pubertal, and 5 late/postpubertal) SAT layers were measured by means of the optical device Lipometer. Fat mass (FM) was estimated indirectly by means of bioelectrical impedance. Leptin and insulin were determined by means of radioimmunoassays. All measurements were performed before (pre) and after (post) 3 weeks of low-caloric diet and physical training. At the beginning of the study, there were significant correlations for all estimates of adiposity and leptin (0.67 to 0.79; P < 0.0001). Five SAT layers from the upper body and the trunk (0.48 to 0.67; P < 0.01) but none from the abdominal region and lower extremities were correlated with leptin. FM together with SAT layers 4-upper back and 8-lower abdomen (negative slope) explained 79% of the variation in pre leptin values (P < 0.0001). The weight-loss program significantly reduced leptin (P < 0.0001), insulin (P = 0.04), estimates of adiposity (P < 0.0001), and SAT layers 4-upper back (P = 0.0006), 11-front thigh, 13-rear thigh, and 14-inner thigh (P between <0.03 and <0.01). Although significant, the reductions in the four SAT layers were small. Estimated fat-free mass was significantly increased after three weeks (P < 0.05). Changes in SAT layers from the upper extremities and from the trunk were inversely correlated to the decrease in leptin (P between <0.05 and <0.001). Initial leptin was the best correlate of the decrease in leptin (adj. R(2) = 0.815; P < 0.0001). However, when only changes in adiposity and insulin were considered in the regression model, changes in insulin contributed to the fall in leptin (adj. R(2) = 0.23; P = 0.004). When changes in SAT layers were added to the model, changes in SAT layers 2-triceps and 10-hip (negative slopes) contributed to the decrease in leptin (adj. R(2) = 0.48; P < 0.0001). After weight loss, correlations between estimates of post adiposity and post leptin (0.40, P = 0.01 to 0.57, P = 0.0005) were lower compared with pre values. SAT layers 4-upper back and 3-biceps contributed independently to post leptin values (adj. R(2) = 0.50; P < 0.0001). It is suggested that fat mass and SAT layers from the upper body are the main determinants of leptin in obese girls before weight loss. The diet and sports intervention program reduced leptin independent of the reduction in adiposity. The distribution of subcutaneous fat might be a stable correlate of circulating leptin after a short-term reduction in energy intake. Am. J. Hum. Biol. 12:803-813, 2000. Copyright 2000 Wiley-Liss, Inc.