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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
HCG: How much is safe to use?
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<blockquote data-quote="DragonBits" data-source="post: 137966" data-attributes="member: 18023"><p>But that implies for some HCG increases estrogen more than would be indicated by the increase in testosterone. </p><p></p><p>Meaning if you bring your TT to 1200 via testosterone cypionate , you get less estrogen than if you increase your TT to 1200 via testosterone cypionate and HCG.</p><p></p><p>Which doesn't make sense to me unless either people aren't being very exacting in their measurements (not really the same levels of TT for each protocol), or there is something else going on which we aren't aware of.</p><p></p><p>There is also the fact that TC will give you a different "waveform" of TT rise Vs your testicles. However, I would think the sharp quick rise from a TC injection would result in more E2 and HCT than a similar rise from your testicles.</p><p></p><p>Correct me if I am wrong, but HCG isn't often used in men outside of TRT, once in a while for fertility reason, so it isn't well studied.</p><p></p><p>Also, I have read HCG is 5 times more potent than LH in some situations, while LH is more potent in other situations, but it's beyond me to really understand this.</p><p></p><p>--------------------------------------------------------------</p><p>LH and hCG Action on the Same Receptor Results in Quantitatively and Qualitatively Different Intracellular Signalling</p><p></p><p>Abstract</p><p></p><p>Human luteinizing hormone (hLH) and chorionic gonadotropin (hCG) act on the same receptor (LHCGR) but it is not known whether they elicit the same cellular and molecular response. This study compares for the first time the activation of cell-signalling pathways and gene expression in response to hLH and hCG. Using recombinant hLH and recombinant hCG we evaluated the kinetics of cAMP production in COS-7 and hGL5 cells permanently expressing LHCGR (COS-7/LHCGR, hGL5/LHCGR), as well as cAMP, ERK1/2, AKT activation and progesterone production in primary human granulosa cells (hGLC). The expression of selected target genes was measured in the presence or absence of ERK- or AKT-pathways inhibitors. In COS-7/LHCGR cells, hCG is 5-fold more potent than hLH (cAMP ED50: 107.1±14.3 pM and 530.0±51.2 pM, respectively). hLH maximal effect was significantly faster (10 minutes by hLH; 1 hour by hCG). In hGLC continuous exposure to equipotent doses of gonadotropins up to 36 hours revealed that intracellular cAMP production is oscillating and significantly higher by hCG versus hLH. Conversely, phospho-ERK1/2 and -AKT activation was more potent and sustained by hLH versus hCG. ERK1/2 and AKT inhibition removed the inhibitory effect on <em>NRG1</em> (neuregulin) expression by hLH but not by hCG; ERK1/2 inhibition significantly increased hLH- but not hCG-stimulated <em>CYP19A1</em> (aromatase) expression. We conclude that: i) hCG is more potent on cAMP production, while hLH is more potent on ERK and AKT activation; ii) hGLC respond to equipotent, constant hLH or hCG stimulation with a fluctuating cAMP production and progressive progesterone secretion; and iii) the expression of hLH and hCG target genes partly involves the activation of different pathways depending on the ligand. Therefore, the LHCGR is able to differentiate the activity of hLH and hCG.</p><p></p><p><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3465272/" target="_blank">LH and hCG Action on the Same Receptor Results in Quantitatively and Qualitatively Different Intracellular Signalling</a></p><p></p><p>Honestly, I have no idea what cAMP production is nor what that all means. Can anyone explain what cAMP is?</p></blockquote><p></p>
[QUOTE="DragonBits, post: 137966, member: 18023"] But that implies for some HCG increases estrogen more than would be indicated by the increase in testosterone. Meaning if you bring your TT to 1200 via testosterone cypionate , you get less estrogen than if you increase your TT to 1200 via testosterone cypionate and HCG. Which doesn't make sense to me unless either people aren't being very exacting in their measurements (not really the same levels of TT for each protocol), or there is something else going on which we aren't aware of. There is also the fact that TC will give you a different "waveform" of TT rise Vs your testicles. However, I would think the sharp quick rise from a TC injection would result in more E2 and HCT than a similar rise from your testicles. Correct me if I am wrong, but HCG isn't often used in men outside of TRT, once in a while for fertility reason, so it isn't well studied. Also, I have read HCG is 5 times more potent than LH in some situations, while LH is more potent in other situations, but it's beyond me to really understand this. -------------------------------------------------------------- LH and hCG Action on the Same Receptor Results in Quantitatively and Qualitatively Different Intracellular Signalling Abstract Human luteinizing hormone (hLH) and chorionic gonadotropin (hCG) act on the same receptor (LHCGR) but it is not known whether they elicit the same cellular and molecular response. This study compares for the first time the activation of cell-signalling pathways and gene expression in response to hLH and hCG. Using recombinant hLH and recombinant hCG we evaluated the kinetics of cAMP production in COS-7 and hGL5 cells permanently expressing LHCGR (COS-7/LHCGR, hGL5/LHCGR), as well as cAMP, ERK1/2, AKT activation and progesterone production in primary human granulosa cells (hGLC). The expression of selected target genes was measured in the presence or absence of ERK- or AKT-pathways inhibitors. In COS-7/LHCGR cells, hCG is 5-fold more potent than hLH (cAMP ED50: 107.1±14.3 pM and 530.0±51.2 pM, respectively). hLH maximal effect was significantly faster (10 minutes by hLH; 1 hour by hCG). In hGLC continuous exposure to equipotent doses of gonadotropins up to 36 hours revealed that intracellular cAMP production is oscillating and significantly higher by hCG versus hLH. Conversely, phospho-ERK1/2 and -AKT activation was more potent and sustained by hLH versus hCG. ERK1/2 and AKT inhibition removed the inhibitory effect on [I]NRG1[/I] (neuregulin) expression by hLH but not by hCG; ERK1/2 inhibition significantly increased hLH- but not hCG-stimulated [I]CYP19A1[/I] (aromatase) expression. We conclude that: i) hCG is more potent on cAMP production, while hLH is more potent on ERK and AKT activation; ii) hGLC respond to equipotent, constant hLH or hCG stimulation with a fluctuating cAMP production and progressive progesterone secretion; and iii) the expression of hLH and hCG target genes partly involves the activation of different pathways depending on the ligand. Therefore, the LHCGR is able to differentiate the activity of hLH and hCG. [URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3465272/']LH and hCG Action on the Same Receptor Results in Quantitatively and Qualitatively Different Intracellular Signalling[/URL] Honestly, I have no idea what cAMP production is nor what that all means. Can anyone explain what cAMP is? [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
HCG: How much is safe to use?
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