Department of Endocrinology, Royal Hospital for Sick Children, Glasgow, UK.
Clin Endocrinol (Oxf). 2014 Jan;80(1):85-91. doi: 10.1111/cen.12263. Epub 2013 Jul 11.
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.
肥胖与骨量呈正相关。这被认为是由于骨骼受到机械负荷,以及控制食欲和体重的各种激素和脂肪细胞因子(如瘦素)的作用,其中一些直接影响骨量。然而,关于脂肪量与儿童骨量之间的关系存在相互矛盾的报告。动物研究表明,中央瘦素信号受损会导致骨量增加。下丘脑损伤可导致异常的中央瘦素作用,从而导致肥胖的发展。
本研究旨在探讨下丘脑单纯性肥胖儿童的体成分与骨量的关系,并结合脂肪细胞因子瘦素和脂联素的作用。
这是一项对三组儿童(下丘脑肥胖组[HO]、先天性垂体功能减退症组[CH]和单纯性肥胖组[SO])进行的横断面研究。
共 65 名儿童(HO = 26 名[11 名男性],CH = 17 名[8 名男性],SO = 22 名[15 名男性])通过双能 X 射线吸收法评估体成分,并测量血清瘦素和脂联素。在调整了各组间身体大小差异的骨密度(BMD)后,骨量未见明显差异。与 SO 组相比,HO 组的瘦素和脂联素水平显著升高(P < 0.01,P < 0.05)。
肥胖与骨量增加有关;然而,这种关系很复杂。尽管存在高瘦素血症,但 HO 组并未出现骨量增加。这可能是由于其他因素的影响,如脂联素、异常的下丘脑信号、垂体激素缺乏以及下丘脑正常内稳态机制的破坏。