Obesity has been associated with a positive influence on bone mass. This is thought to be due to a mechanical load exerted on the skeleton, together with various hormones and adipocytokines that control appetite and weight, such as leptin, some of which directly affect bone mass. However, there are conflicting reports of the association between fat mass and bone mass in children. Animal studies demonstrate increased bone mass where there is impaired central leptin signalling. Hypothalamic damage can cause abnormal central leptin action, which contributes to the development of obesity.


The objective of this study was to investigate the relationship between body composition and bone mass in hypothalamic and simple childhood obesity, in conjunction with the effect of the adipocytokines, leptin and adiponectin.


This was a cross-sectional study of three groups of children, those with hypothalamic obesity (HO), those with congenital hypopituitarism (CH) and those with simple obesity (SO).


A total of 65 children (HO = 26 [11 males], CH = 17 [eight males] and SO = 22 [15 males]) had body composition assessed using dual-energy X-ray absorptiometry together with measurement of serum leptin and adiponectin. No significant differences were seen in bone mass once bone density (BMD) was adjusted for differences in body size between groups. Significantly elevated levels of leptin and adiponectin were seen in the HO group compared with the SO group (P < 0·01, P < 0·05, respectively).


Adiposity is associated with increased bone mass; however, this relationship is complex. Despite the presence of hyperleptinaemia, increased bone mass in the HO group was not seen. This may be due to the effects of other factors such as adiponectin, abnormal hypothalamic signalling, pituitary hormone deficiencies and disruption of normal homoeostatic mechanisms within the hypothalamus.