Regulation of growth hormone secretion and messenger ribonucleic acid accumulation in human somatotropinoma cells in vitro.
Davis. J R JR; Wilson. E M EM; Vidal. M E ME; Johnson. A P AP; Lynch. S S SS; Sheppard. M C MC
Key Findings
- GRF‑1‑29 increased GH release (30‑97% above baseline) in three out of four tumor samples and sometimes raised GH mRNA levels.
- Somatostatin strongly inhibited GH secretion but did not reduce GH mRNA, indicating a disconnect between release and gene transcription.
- Forskolin stimulated both GH release and mRNA in tumors that responded to GRF, while other agents (phorbol ester) had inconsistent effects, highlighting high variability between tumors.
Practical Outcomes
- For biohackers, GRF‑1‑29 can boost GH secretion, but the response may differ between individuals, so results are not guaranteed. The data come from tumor cells in a dish, so they don’t directly tell you the best dose or schedule for healthy people. Use this as a reminder that personal variability is expected and that more human‑focused studies are needed before fine‑tuning protocols.
Summary
The study looked at how a GH‑releasing peptide (GRF‑1‑29) and other drugs affect growth‑hormone release from human pituitary tumor cells. GRF‑1‑29 raised GH secretion in most of the tumors tested, but the effect on the hormone’s gene activity (mRNA) was weaker and varied a lot. Other compounds like somatostatin and bromocriptine blocked GH release without changing mRNA, and forskolin acted like GRF only in the most responsive tumors.
Abstract
GH secretion and mRNA levels were measured in cultured cells obtained from six human pituitary somatotroph tumors to investigate their hormonal and intracellular regulation. The responses were variable between tumors, but, in general, mRNA levels were less responsive than GH release to in vitro manipulation. GH-releasing factor [GRF-(1-29) amide; 10 nM] increased GH release and mRNA levels in three of four tumors tested to 30-97% above control values, but the fourth tumor was unresponsive. Somatostatin (1 microM) inhibited GH release significantly in four of the six cases, to 35-79% of control levels, but had no inhibitory effect on GH mRNA accumulation, in contrast to earlier studies on rat pituitary tissue. Bromocriptine (100 nM) likewise inhibited GH release (50-75% of control), but not GH mRNA levels, in the four tumors tested. Forskolin (10 microM; used to activate adenylate cyclase) stimulated GH release and mRNA levels in the two cases that responded most clearly to GRF, but had no significant effect in the other tumors; however, the phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (100 nM) had no consistent effect on mRNA levels despite stimulating secretion in four of six cases. Thus, there was considerable variation in responses among the tumors tested; however, the responsiveness to GRF was approximately paralleled by that to forskolin, consistent with the suggestion that adenylate cyclase activity and responsiveness are variable among these tumors. Furthermore, the divergent effects of somatostatin on GH release and mRNA suggest uncoupling between its receptor and transcriptional regulatory mechanisms.
Study Information
pubmed
1989
10.1210/jcem-69-4-704