Key result
In cultured mouse pituitary cells, GH treatment significantly increased IGF-I mRNA levels, while IGF-I treatment decreased GH mRNA levels and increased POMC mRNA levels.
Effect estimate: 1.5- to 2.1-fold increase in IGF-I mRNA with GH; 0.5- to 0.7-fold decrease in GH mRNA and 1.8-fold increase in POMC mRNA with IGF-I
p-value: p=<0.05
In mouse pituitary cells, GH stimulates IGF-I expression, while IGF-I suppresses GH expression and stimulates POMC expression, indicating an intrapituitary regulatory feedback loop.
Mouse pituitary feedback data extend rodent models; leaves open human GH/IGF-I/POMC relevance.
IGF-I is expressed in somatotrophs, and IGF-I receptors are expressed in most somatotrophs and some corticotrophs in the mouse pituitary gland. Our recent study demonstrated that IGF-I stimulates the proliferation of corticotrophs in the mouse pituitary. These results suggested that somatotrophs regulate corticotrophic functions as well as somatotrophic functions by the mediation of IGF-I molecules. The present study aimed to clarify factors regulating pituitary IGF-I expression and also the roles exerted by IGF-I within the mouse anterior pituitary gland. Mouse anterior pituitary cells were isolated and cultured under serum-free conditions. GH (0.5 or 1 microg/ml), ACTH (10(-8) or 10(-7) M), GH-releasing hormone (GHRH; 10(-8) or 10(-7) M), dexamethasone (DEX; 10(-8) or 10(-7) M) and estradiol-17beta (e2; 10(-11) or 10(-9) M) were given for 24 h. IGF-I mRNA levels were measured using competitive RT-PCR, and GH and pro-opiomelanocortin (POMC) mRNA levels were measured using Northern blotting analysis. GH treatment significantly increased IGF-I mRNA levels (1.5- or 2.1-fold). ACTH treatment did not alter GH and IGF-I mRNA levels. IGF-I treatment decreased GH mRNA levels (0.7- or 0.5-fold), but increased POMC mRNA levels (1.8-fold). GH treatment (4 or 8 microg/ml) for 4 days increased POMC mRNA levels. GHRH treatment increased GH mRNA levels (1.3-fold), but not IGF-I mRNA levels. DEX treatment significantly decreased IGF-I mRNA levels (0.8-fold). e2 treatment did not affect IGF-I mRNA levels. GH receptor mRNA, probably with GH-binding protein mRNA, was detected in somatotrophs, and some mammotrophs and gonadotrophs by in situ hybridization using GH receptor cDNA as a probe. These results suggested that IGF-I expression in somatotrophs is regulated by pituitary GH, and that IGF-I suppresses GH expression and stimulates POMC expression at the transcription level. Pituitary IGF-I produced in somatotrophs is probably involved in the regulation of somatotroph and corticotroph functions.
No takes yet. Share an insight, caveat, or question.
Honda et al. (2003) studied Normal physiology (mouse pituitary). IGF-I and GH vs. Control (no hormone treatment) was evaluated on IGF-I, GH, and POMC mRNA levels (1.5- to 2.1-fold increase in IGF-I mRNA with GH; 0.5- to 0.7-fold decrease in GH mRNA and 1.8-fold increase in POMC mRNA with IGF-I, p=<0.05). In cultured mouse pituitary cells, GH treatment significantly increased IGF-I mRNA levels, while IGF-I treatment decreased GH mRNA levels and increased POMC mRNA levels.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: