Hypothalamic tumor involvement and familial disposition for obesity are risk factors for the development of severe obesity in patients with craniopharyngioma. As weight gain starts early after diagnosis and severe obesity causes a reduction in QoL, early therapeutic efforts should be considered in patients at risk. To confirm our results the prospective multicenter study Kraniopharyngeom 2000 on children and adolescents with craniopharyngioma was initiated (www.kraniopharyngeom.com).

Patients with childhood-onset craniopharyngioma (CP) often suffer from obesity. We evaluated two important etiological factors of obesity development, energy intake and physical activity. Energy intake was supposed to be high due to a disturbed hypothalamic regulation of appetite. We used a validated nutritional diary to determine the 1-wk food intake in 27 CP patients (12 with intrasellar tumors and 15 with hypothalamic tumors) and 1027 controls who were a representative sample of the 7- to 16-yr-old German population. In 2 accelerometry settings, we determined movement counts indicating physical activity. Nineteen CP patients were comparable to 26 controls for age and body mass index. One setting was a clinical one during weight reduction; the other was an out-patient setting. Daily energy intake was 1916 +/- 677 kcal (mean +/- SD) in intrasellar CP patients, 2075 +/- 877 kcal in hypothalamic CP patients, and 2476 +/- 815 kcal in non-CP controls. Patients suffering from CP showed fewer movement registrations [clinical setting, 228 vs. 298 cpm for obese controls (P = 0.01); out-patient setting, 228 vs. 282 cpm for controls (P = 0.08)]. Differences were most pronounced during leisure time (382 cpm in CP patients vs. 546 cpm in obese controls; P = 0.002; clinical setting). Our findings suggest that reduced physical activity, rather than increased energy intake, in CP patients is responsible for the obesity development noted in these subjects.

PYY is negatively correlated to the degree of overweight, with reduced values in obese compared with normal-weight children. Decreased PYY levels could predispose subjects to develop obesity. Our results indicate that low pretreatment PYY levels that increase during weight loss may be a predictor of maintained weight loss.

Objective: Little is known concerning pancreatic polypeptide (PP) in weight loss and in childhood obesity. Methods: Fasting PP, leptin and insulin concentrations were determined in 38 obese children and compared with 35 lean children of the same age, gender and pubertal stage. Furthermore, changes of PP concentrations over a 1-year period were analyzed in the obese children participating in a weight loss intervention program. Results: Obese children had significantly (Po0.01) lower PP, and higher leptin and insulin levels compared to lean children. In multiple linear regression analysis, PP was significantly negatively correlated to body mass index (Po0.01), but not to leptin, insulin, age, gender and pubertal stage. Changes of PP did not significantly correlate to changes of insulin (r ¼ 0.07, P ¼ 0.343) and leptin (r ¼ À0.02, P ¼ 0.459). The substantial weight loss in 17 children led to a significant (Po0.05) increase in PP and decrease in insulin and leptin. In the 21 children without substantial weight loss, there were no significant changes in PP, insulin and leptin. Conclusions: PP concentrations are decreased in obese children and independent of age, gender, pubertal stage, leptin and insulin. The decrease of PP in obese children normalized after weight loss. Therefore, low PP concentrations reflect the overweight status, rather than cause it.