Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Department of Biomaterials, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Endocrinology. 2021 Jun 1;162(6). doi: 10.1210/endocr/bqab053.
In healthy conditions, prepubertal growth follows an individual specific growth channel. Growth hormone (GH) is undoubtedly the major regulator of growth. However, the homeostatic regulation to maintain the individual specific growth channel during growth is unclear. We recently hypothesized a body weight sensing homeostatic regulation of body weight during adulthood, the gravitostat. We now investigated if sensing of body weight also contributes to the strict homeostatic regulation to maintain the individual specific growth channel during prepubertal growth. To evaluate the effect of increased artificial loading on prepubertal growth, we implanted heavy (20% of body weight) or light (2% of the body weight) capsules into the abdomen of 26-day-old male rats. The body growth, as determined by change in biological body weight and growth of the long bones and the axial skeleton, was reduced in rats bearing a heavy load compared with light load. Removal of the increased load resulted in a catch-up growth and a normalization of body weight. Loading decreased hypothalamic growth hormone releasing hormone mRNA, liver insulin-like growth factor (IGF)-1 mRNA, and serum IGF-1, suggesting that the reduced body growth was caused by a negative feedback regulation on the somatotropic axis and this notion was supported by the fact that increased loading did not reduce body growth in GH-treated rats. Based on these data, we propose the gravitostat hypothesis for the regulation of prepubertal growth. This states that there is a homeostatic regulation to maintain the individual specific growth channel via body weight sensing, regulating the somatotropic axis and explaining catch-up growth.
在健康的条件下，青春期前的生长遵循个体特有的生长通道。生长激素（GH）无疑是生长的主要调节因子。然而，在生长过程中维持个体特有的生长通道的内稳态调节尚不清楚。我们最近假设了一种在成年期通过体重感知来维持体重的内稳态调节，即重立场。我们现在研究了体重感知是否也有助于严格的内稳态调节，以维持青春期前生长过程中的个体特有的生长通道。为了评估增加人工负荷对青春期前生长的影响，我们将重（体重的 20%）或轻（体重的 2%）胶囊植入 26 天大的雄性大鼠的腹部。与轻负荷组相比，承载重负荷的大鼠的身体生长（通过生物体重变化和长骨和轴骨的生长来确定）减少。去除增加的负荷会导致追赶生长和体重正常化。负荷降低了下丘脑生长激素释放激素 mRNA、肝脏胰岛素样生长因子（IGF-1）mRNA 和血清 IGF-1，表明体重减轻是由于对生长激素轴的负反馈调节所致，这一观点得到了以下事实的支持：增加的负荷不会减少 GH 治疗大鼠的体重生长。基于这些数据，我们提出了重力场假说来调节青春期前的生长。这表明存在一种通过体重感知来维持个体特有的生长通道的内稳态调节，调节生长激素轴，并解释追赶生长。
