Hello Robin!
Your sense is correct that the GH effect effects sex hormone secretion!
- In young women, IGF-1 not only acts on theca cells of the ovary to promote androgen production, but also acts synergistically with FSH to increase aromatase activity, thereby stimulating estrogen production
- GH release increases IGF-1 production. It is believed that declining IGF-1 leads to reproductive senescence, so increasing IGF-1 can possibly extend reproduction!
- In young individuals, GH contributes to the regulation of puberty and fertility via HPG axis stimulation through changes in the levels of SS and/or gonadotropin secretion
- GH specifically acts on its receptors in the ovary to promote steroidogenesis and gametogenesis via gonadotropin-independent stimulation of progesterone (P4) and estrogen (E2), inhibition of follicular apoptosis and upregulation of ovarian LH receptors
- Treatment with GH has been shown to reinstate normal ovarian activity in GH insufficient girls and women, who suffer from delayed puberty, abnormal menstrual cycling and infertility
- GH administration to women with amenorrhea increases plasma E2 levels, LH pulse frequency and reduces LH pulse amplitude
Growth Hormone:
- 191 amino acid protein that binds to the growth hormone receptor (GHR)
- GHR mainly is detected in the liver, but has been found in the ovary and testes
- GH and IGF modulate the following signal transduction pathways:
- MAP kinase/ERK
- Jak/STAT
- PI3K/AKT
For further in-depth review please go to the Hormone Therapies Foundation course. This gives an excellent review of cellular pathways with Growth hormone and IGF-1 influences on the ovary and the testes.
Here is a brief summary below:
So, with the injection of a GHRH/GHRP like the CJC1295/Ipamorelin you are using with this patient these peptides set off a cascade of endogenous GH release and because of the Ipamorelin there is no somatostatin inhibition on this release from the anterior pituitary.
GH has an effect on every cell that has a GH- receptors (GHR) .GH and IGF-1 will activate kisspeptin which is released in the hypothalamus and activates Gonadotropin releasing Hormone (GnRH) which activates LH and FSH release in the anterior pituitary. Also, GnRH is also independently activated by IGF-1.
GH, FSH and LH signal the ovary. This induces thecal cells, production of sex steroids mainly estradiol which influences the ovary and in general circulation leads to pituitary LH release and with further Somatostatin inhibition leading to more GH release.
If you take a look at this effect in older females who are post-menopausal you can see this study confirmed that GH does not alter sex steroid production and has no effect on LH. Even with increases in IGF-1 there are no effects on the HPG (hypothalamus-Pituitary-Gonadal) axis as we see in pre and perimenopausal females. This can certainly be attributed to the senescence that takes place in the astrocytes of the hypothalamus where estrogen signaling promotes progesterone production and eventual LH release.
Resources:
Muniyappa R, Sullivan SD, Tella SH, Abel BS, Harman SM, Blackman MR. Effects of growth hormone administration on luteinizing hormone secretion in healthy older men and women. Physiol Rep. 2017;5(23):e13516. doi:10.14814/phy2.13516
This is a great reference article that discusses the Growth Hormone and Insulin-Like Growth Factor Action in Reproductive Tissues: Ipsa, Emina, Vinicius F. Cruzat, Jackob N. Kagize, John L. Yovich, and Kevin N. Keane. “Growth Hormone and Insulin-Like Growth Factor Action in Reproductive Tissues.” Frontiers in Endocrinology 10 (2019): 777. https://doi.org/10.3389/fendo.2019.00777.
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