Because fT3 and TSH were moderately increased in obese children and weight loss led to a reduction, the elevation of these hormones seems to be rather a consequence of obesity than a cause of obesity. Because fT3 and TSH were both increased in obesity and thyroid hormones were not associated to lipids, we put forward the hypothesis that there is no necessity for thyroxine treatment.

Long-term multidisciplinary intervention led to a reduction in SDS-BMI in most of the obese children 1 y after the end of the intervention. Reduction in SDS-BMI was accompanied by an improvement in CVD risk factors.

Background/Aims: The aim of this study was to analyze thyroid hormones in female adolescents with obesity and anorexia nervosa (AN) before and after normalization of weight. Methods: Thyroid-stimulating hormone (TSH), fT3, and fT4 were determined in 100 obese girls, 32 normal-weight girls and 20 girls with AN aged 14–18 years at baseline and 1 year later. Additionally, leptin, insulin, and the insulin resistance index HOMA were analyzed in the obese and normal-weight girls. Results: TSH and fT3 levels of girls with AN were significantly lower compared to TSH concentrations of normal-weight girls, while TSH and fT3 levels of the obese girls were significantly higher. The 21 obese females with weight loss >5% demonstrated a significant decrease in fT3 and TSH, while the 9 adolescents with AN and weight gain >5% showed a significant increase in fT3 and TSH. Insulin and HOMA were not significantly correlated to TSH, fT3 and fT4, while leptin was correlated to TSH and fT3 in both cross-sectional and longitudinal analysis. Conclusions: Thyroid function seems to be reversibly related to weight status with increased TSH and fT3 concentrations in obesity and decreased TSH and fT3 levels in AN. We hypothesize that leptin may be the link between weight status and TSH.

Since the prevalence of the MS varied widely in overweight children and adolescents depending on the proposed definition used, an internationally accepted uniform definition of the MS is necessary to compare different populations and studies.

Objective: The roles of vitamin D and parathyroid hormone (PTH) are discussed controversially in obesity, and studies of these hormones in obese children are limited. Therefore, we studied the relationships between PTH, 1,25-dihydroxy-vitamin D (1,25-OH Vit D), 25-hydroxy-vitamin D (25-OH Vit D), weight status, and insulin sensitivity before and after weight loss in obese children. Methods: Fasting serum PTH, 1,25-OH Vit D, 25-OH Vit D, inorganic phosphate, calcium, alkaline phosphatase (AP), insulin, glucose, and weight status (SDS-BMI and percentage body fat) were determined in 133 obese children (median age 12.1 years) and compared with 23 non-obese children. Furthermore, these parameters were analyzed in 67 obese children before and after participating in a 1-year obesity intervention program. Results: Obese children had significantly (P!0.001) higher PTH and lower 25-OH Vit D concentrations compared with non-obese children, while calcium, phosphate, AP, and 1,25-OH Vit D did not differ significantly. Changes of PTH (rZ0.23, PZ0.031) and 25-OH Vit D (rZK0.27, PZ0.013) correlated significantly with changes of SDS-BMI, but not with changes of insulin sensitivity (homeostasis model assessment; HOMA-B%). Reduction of overweight in 35 children led to a significant (P!0.01) decrease of PTH concentrations and an increase in 25-OH Vit D levels. Conclusions: PTH levels were positively and 25-OH Vit D concentrations were negatively related to weight status. Since these alterations normalized after weight loss, these changes are consequences rather than causes of overweight. A relationship between PTH, vitamin D, and insulin sensitivity based on the HOMA index was not found in obese children. Further longitudinal clamp studies are neccessary to study the relationship between vitamin D and insulin sensitivity. European Journal of Endocrinology 157 225-232Introduction Vitamin D and parathyroid hormone (PTH) are well known for their essential role in bone metabolism and calcium homeostasis. The main sources of vitamin D are ergocalciferol and cholecalciferol, the former normally available in food and the latter produced in the skin by u.v. radiation of 7-dehydrocholesterol. Both of these compounds are hydroxylated in the liver to 25-hydroxyvitamin D (25-OH Vit D), which is the major circulating metabolite precursor to the hormonally active form, 1,25-dihydroxy-vitamin D (1,25-OH Vit D).It has become increasingly clear that the vitamin D endocrine system is related to obesity in adults. Obesity has been found to be associated with lower levels of serum 25-OH Vit D (1-5) and higher levels of serum PTH (1,(5)(6)(7)(8). A low vitamin D intake was associated with increased body mass index (BMI) (9). PTH has been postulated as an independent predictor of obesity (7). Overweight as a consequence of elevated serum PTH was explained by several mechanisms (10, 11): PTH stimulates the renal hydroxylation of 25-OH Vit D to its active form, 1,25-OH Vit D, which in turn elevates the calcium influx into adipocytes. In these cell...