W
waddles
Iron
- Joined
- Oct 2, 2025
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I see a lot of the younger generation always talking about HGH, somatropin, or any of it's analogs: CJC-1293, Ibutamoren, GHRP2, etc. I'd firstly like to start with nothing I say is medical advise and should be taken with a grain of salt. I'd like to talk about the more counteractive part of Growth Hormone, GHIH, Growth Hormone Inhibiting-Hormone, more notable SST (Somastatin). GHIH is secreted from the hypothalamus, and elsewhere. It acts directly on the pituitary gland, by telling the gland to stop secreting GH, which gives the GH the "pulse". Alongside this, it also halts the secretion of TSH, Thyroid-Stimulating Hormone, which stimulates the thyroid gland, by binding to the TSHR, a G like protein receptor on top the follicular cells (These proteins are either Gs but also sometimes Gq), this leads to the increase of cAMP pathway, essentially the activation of PKA (Protein Kinase A) alongside with other phosphorylation transcript factors -> inc of size of thyroid gland, NIS expression, thyroglobulin production, TPO activity, with other minute changes. If those proteins were to couple with Gq proteins, we would see a increase in production of IP3 + DAG -> Ca2+ intracellular / more thyroid hormone secretion. So what does this do over all? Well it produces the T3 and T4 hormones, and releases it back into the bloodstream. So why do we want a upkeep of T3/T4, when the health of the TSH or the gland lacks T3 drops leading for little to nothing to bind to thyroid receptor hormone 1, which leads to osteoblast and osteoclast -> euthyroid sick syndrome.
Insulin and glucagon work somewhat together creating a negative feedback loop. Firstly, SSTR2 binds to alpha-cells (glucagon) and SSTR5 binds to beta-cells (insulin), which inhibits or halts there actions temporally. Gi receptors get activated, leads to lowering of cAMP, reducing Ca2+ intracellular, and exocytosis of those hormones. But insulin and glucagon (This is to a lesser degree), however what I said there was a way to "stop" or "halt" this? I can later add studies and of course go into more detail with this subject matter and many more things that are scarcely mentioned within gym communities or looksmaxxing communities. With that all being said, if you did read any of that and just came here for the solution, BIM-23627, it works by binding to the SSTR in some studies I have found it works fully by inhibiting GHIH, and in others partially. By blocking somatostatin, BIM-23627 can increase GH secretion because it removes the natural inhibition of GHIH. Now it was also shown to have a slight affect on free/total testosterone. With all of that being said, those are based for theoretical human based data upon rats, in experimental settings.
I can go deeper into these things if needed, and so on.
Insulin and glucagon work somewhat together creating a negative feedback loop. Firstly, SSTR2 binds to alpha-cells (glucagon) and SSTR5 binds to beta-cells (insulin), which inhibits or halts there actions temporally. Gi receptors get activated, leads to lowering of cAMP, reducing Ca2+ intracellular, and exocytosis of those hormones. But insulin and glucagon (This is to a lesser degree), however what I said there was a way to "stop" or "halt" this? I can later add studies and of course go into more detail with this subject matter and many more things that are scarcely mentioned within gym communities or looksmaxxing communities. With that all being said, if you did read any of that and just came here for the solution, BIM-23627, it works by binding to the SSTR in some studies I have found it works fully by inhibiting GHIH, and in others partially. By blocking somatostatin, BIM-23627 can increase GH secretion because it removes the natural inhibition of GHIH. Now it was also shown to have a slight affect on free/total testosterone. With all of that being said, those are based for theoretical human based data upon rats, in experimental settings.
I can go deeper into these things if needed, and so on.