| First Author | Wallenius K | Year | 2001 |
| Journal | Endocrinology | Volume | 142 |
| Issue | 11 | Pages | 4762-70 |
| PubMed ID | 11606442 | Mgi Jnum | J:72793 |
| Mgi Id | MGI:2153610 | Doi | 10.1210/endo.142.11.8478 |
| Citation | Wallenius K, et al. (2001) Liver-derived igf-i regulates gh secretion at the pituitary level in mice. Endocrinology 142(11):4762-70 |
| abstractText | We have reported that liver-specific deletion of IGF-I in mice (LI-IGF-I-/-) results in decreased circulating IGF-I and increased GH levels. In the present study, we determined how elimination of hepatic IGF-I modifies the hypothalamic-pituitary GH axis to enhance GH secretion. The pituitary mRNA levels of GH releasing factor (GHRF) receptor and GH secretagogue (GHS) receptor were increased in LI-IGF-I-/- mice, and in line with this, their GH response to ip injections of GHRF and GHS was increased. Expression of mRNA for pituitary somatostatin receptors, hypothalamic GHRF, somatostatin, and neuropeptide Y was not altered in LI-IGF-I-/- mice, whereas hypothalamic IGF-I expression was increased. Changes in hepatic expression of major urinary protein and the PRL receptor in male LI-IGF-I-/- mice indicated an altered GH release pattern most consistent with enhanced GH trough levels. Liver weight was enhanced in LI-IGF-I-/- mice of both genders. In conclusion, loss of liver-derived IGF-I enhances GH release by increasing expression of pituitary GHRF and GHS receptors. The enhanced GH release in turn affects several liver parameters, in line with the existence of a pituitary-liver axis. |
