| Abstrakt: |
Hyperprolactinemia has been related to the pathogenesis of impaired glucose tolerance and hyperinsulinemia resulting in overt insulin resistance. Human secreted excess glucocorticoid can get Cushing's syndrome to lead to dyslipidemia, and insulin resistance/type 2 diabetes. Prolactin (PRL) and glucocorticoid might interfere with each other. Hence, this research directed to elucidate the influence of hyperprolactinemia on the release of corticosterone by zona fasciculata-reticularis (ZFR) cells from ovariectomized rats. For hyperprolactinemia, two rat anterior pituitary glands (Aps), or a fragment of cerebral cortex (Cx) for each rat were transplanted under the kidney capsule and mice were kept for 2 months prior to euthanasia. The ZFR cells derived from Cx-grafted and Ap-grafted groups were incubated in the presence of adrenocorticotropic hormone (ACTH), forskolin, IBMX, 8-bromo-cyclic 3': 5'-adenosine monophosphate (8-Br-cAMP), nifedipine, trilostane or steroidogenic precursors at 37oC for 0.5 or 1 hour. The concentration of corticosterone or pregnenolone in the culture media was determined by a radioimmunoassay (RIA). The plasma corticosterone in Ap-grafted rats was significantly elevated than that in Cx-grafted rats. This research demonstrated that hyperprolactinemia enhanced corticosterone production by rat ZFR cells. The action was mediated through enhancing the responsiveness to ACTH stimulation, cyclic AMP (cAMP) cascades, and the activities of steroidogenic enzymes. [ABSTRACT FROM AUTHOR] |
