Mice carrying an RGS-insensitive Gαi2 mutation display growth retardation early after birth. Although the growth hormone (GH)-axis is a key endocrine modulator of postnatal growth, its functional state in these mice has not been characterized. The present study was undertaken to address this issue. Results revealed that pituitary mRNA levels for GH, prolactin (PRL), somatostatin (SST), GH-releasing-hormone receptor (GHRH-R) and GH secretagogue receptor (GHS-R) were decreased in mutants compared to controls. These changes were reflected by a significant decrease in plasma levels of GH, IGF-1 and IGF-binding protein-3 (IGFBP-3). Mutants were also less responsive to GHRH and ghrelin (GhL) on GH stimulation of release from pituitary primary cell cultures. In contrast, they were more sensitive to the inhibitory effect of SST. These data provide the first evidence for an alteration of the functional state of the GH-axis in Gαi2G184S mice that likely contributes to their growth retardation.

携带 RGS 不敏感 Gαi2 突变的小鼠在出生后早期表现出生长迟缓。尽管生长激素 (GH) 轴是出生后生长的关键内分泌调节剂，但其在这些小鼠中的功能状态尚未得到表征。本研究就是为了解决这个问题。结果显示，与对照相比，突变体中 GH、催乳素 (PRL)、生长抑素 (SST)、GH 释放激素受体 (GHRH-R) 和 GH 促分泌素受体 (GHS-R) 的垂体 mRNA 水平降低。这些变化反映在血浆 GH、IGF-1 和 IGF 结合蛋白-3 (IGFBP-3) 水平的显着降低上。突变体对 GHRH 和生长素释放肽 (GhL) 对垂体原代细胞培养物释放的 GH 刺激的反应也较低。相比之下，他们对 SST 的抑制作用更敏感。