| First Author | Omouessi ST | Year | 2021 |
| Journal | Mol Cell Endocrinol | Volume | 521 |
| Pages | 111098 | PubMed ID | 33278490 |
| Mgi Jnum | J:303807 | Mgi Id | MGI:6510769 |
| Doi | 10.1016/j.mce.2020.111098 | Citation | Omouessi ST, et al. (2021) Mice with an RGS-insensitive Galphai2 protein show growth hormone axis dysfunction. Mol Cell Endocrinol 521:111098 |
| abstractText | Mice carrying an RGS-insensitive Galphai2 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 Galphai2G184S mice that likely contributes to their growth retardation. |
