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We examined the effects of GnRH and TRH on inositol phospholipid turnover in 11 endocrinologically inactive pituitary adenomas and 5 prolactinomas. In 9 of the 11 nonsecreting adenomas, GnRH induced a significant increase in inositol phospholipid turnover; of those that responded, increased inositol phospholipid turnover in response to TRH occurred in 6. Neither of the 2 prolactinomas exposed to GnRH responded to GnRH, whereas all 5 prolactinomas responded to TRH. These findings demonstrate the presence of functional GnRH receptors on endocrinologically inactive pituitary adenomas. The phosphatidyl inositol-linked receptor status of these tumors differs from that of prolactinomas. These receptors may offer a possible target for therapeutic intervention in endocrinologically inactive adenomas.
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Levy et al. (1989) studied this question.
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