Agouti-related protein has an inhibitory paracrine role in the rat adrenal gland.

Autor: Dhillo WS; Endocrine Unit, Faculty of Medicine, Imperial College, 6th Floor Commonwealth Building, Hammersmith Hospital, Du Cane Road, London W12 ONN, UK., Small CJ, Gardiner JV, Bewick GA, Whitworth EJ, Jethwa PH, Seal LJ, Ghatei MA, Hinson JP, Bloom SR
Jazyk: angličtina
Zdroj: Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2003 Jan 31; Vol. 301 (1), pp. 102-7.
DOI: 10.1016/s0006-291x(02)02991-1
Abstrakt: alpha-Melanocyte-stimulating-hormone (alpha-MSH) is an agonist at the melanocortin 3 receptor (MC3-R) and melanocortin 4 receptor (MC4-R). alpha-MSH stimulates corticosterone release from rat adrenal glomerulosa cells in vitro. Agouti-related protein (AgRP) an endogenous antagonist at the MC3-R and MC4-R, is expressed in the adrenal gland. We investigated the expression of the MC3-R and MC4-R and the role of AgRP in the adrenal gland. MC3-R and MC4-R expression was detected in rat adrenal gland using RT-PCR. The effect of AgRP on alpha-MSH-induced corticosterone release was investigated using dispersed rat adrenal glomerulosa cells. AgRP administered alone did not affect corticosterone release, but co-administration of AgRP and alpha-MSH attenuated alpha-MSH-induced corticosterone release. To investigate glucocorticoid feedback, adrenal AgRP expression was compared in rats treated with dexamethasone to controls. AgRP mRNA was increased in rats treated with dexamethasone treatment compared to controls. Our findings demonstrate that adrenal AgRP mRNA is regulated by glucocorticoids. AgRP acting via the MC3-R or MC4-R may have an inhibitory paracrine role, blocking alpha-MSH-induced corticosterone secretion.
Databáze: MEDLINE