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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
Kisspeptin-10 as a replacement for compounded HCG?
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<blockquote data-quote="Cataceous" data-source="post: 183121" data-attributes="member: 38109"><p>Also see what the first citation says about the concentrations in general:</p><p></p><p style="margin-left: 20px"><em>The physiological relevance of the KP‐10 concentrations used in our in vitro and in vivo experiments warrants further discussion. First, the concentrations of KP‐10 needed to influence multiple HUVEC, HMDM, and HASMC responses were considerably high (maximum ≈<strong>7400‐fold</strong>) compared with average plasma concentration of KP‐10 (1.35 nmol/L [1.05 ng/mL]) in 28 healthy volunteers (Figure S2B). In the vascular wall, ECs and macrophages generate large amounts of KP‐10 in an autocrine/paracrine manner. Plasma KP‐54 concentration increases by 1000‐ to 10 000‐fold during pregnancy.<a href="https://www.ahajournals.org/doi/10.1161/JAHA.117.005790#jah32173-bib-0041" target="_blank">41</a>Consequently, it is not surprising that local levels of KP‐10 were increased in a similar degree. Second, the concentration of KP‐10 in serum obtained from a healthy human volunteer was 0.32 nmol/L (0.41 ng/mL) in our study. Therefore, the 10% concentration added to culture medium for HMDMs (32 pmol/L) was negligible compared with the concentrations of KP‐10 added. Third, the concentrations of KP‐10 differed in terms of the inflammation responses that they provoked in HUVECs, as well as their influence on monocyte‐HUVEC adhesion, macrophage foam cell formation and effector expression, HASMC migration and proliferation, and ECM production. This likely reflects the different cell types used and their intracellular signals. Fourth, the dose of KP‐10 (12.5 μg/kg per hour) infusion into mice is 9.6‐fold higher compared with its dose (1.3 μg/kg per hour [1.0 nmol/kg per hour]) used in humans.<a href="https://www.ahajournals.org/doi/10.1161/JAHA.117.005790#jah32173-bib-0042" target="_blank">42</a> It is generally accepted to examine the effect of drugs at such a high dose in animal experiments. Fifth, plasma KP‐10 concentration in ApoE−/− mice infused with KP‐10 was significantly higher by 3‐ to 4‐fold (Table <a href="https://www.ahajournals.org/doi/10.1161/JAHA.117.005790#jah32173-tbl-0001" target="_blank">1</a>), which were not as high as we anticipated. KP‐10 might therefore be metabolized, to some degree, in circulating blood.<a href="https://www.ahajournals.org/doi/10.1161/JAHA.117.005790#jah32173-bib-0043" target="_blank">43</a> Last, plasma KP‐10 concentration in ApoE−/− mice infused with KP‐10+P234 was higher compared with KP‐10 alone (Table <a href="https://www.ahajournals.org/doi/10.1161/JAHA.117.005790#jah32173-tbl-0002" target="_blank">2</a>). Given that the amino‐acid sequence of KP‐10 is 70% identical to that of P234 (inactive form), the ELISA kit may detect P234 as KP‐10 (possible cross‐reaction).</em></p></blockquote><p></p>
[QUOTE="Cataceous, post: 183121, member: 38109"] Also see what the first citation says about the concentrations in general: [INDENT][I]The physiological relevance of the KP‐10 concentrations used in our in vitro and in vivo experiments warrants further discussion. First, the concentrations of KP‐10 needed to influence multiple HUVEC, HMDM, and HASMC responses were considerably high (maximum ≈[B]7400‐fold[/B]) compared with average plasma concentration of KP‐10 (1.35 nmol/L [1.05 ng/mL]) in 28 healthy volunteers (Figure S2B). In the vascular wall, ECs and macrophages generate large amounts of KP‐10 in an autocrine/paracrine manner. Plasma KP‐54 concentration increases by 1000‐ to 10 000‐fold during pregnancy.[URL='https://www.ahajournals.org/doi/10.1161/JAHA.117.005790#jah32173-bib-0041']41[/URL]Consequently, it is not surprising that local levels of KP‐10 were increased in a similar degree. Second, the concentration of KP‐10 in serum obtained from a healthy human volunteer was 0.32 nmol/L (0.41 ng/mL) in our study. Therefore, the 10% concentration added to culture medium for HMDMs (32 pmol/L) was negligible compared with the concentrations of KP‐10 added. Third, the concentrations of KP‐10 differed in terms of the inflammation responses that they provoked in HUVECs, as well as their influence on monocyte‐HUVEC adhesion, macrophage foam cell formation and effector expression, HASMC migration and proliferation, and ECM production. This likely reflects the different cell types used and their intracellular signals. Fourth, the dose of KP‐10 (12.5 μg/kg per hour) infusion into mice is 9.6‐fold higher compared with its dose (1.3 μg/kg per hour [1.0 nmol/kg per hour]) used in humans.[URL='https://www.ahajournals.org/doi/10.1161/JAHA.117.005790#jah32173-bib-0042']42[/URL] It is generally accepted to examine the effect of drugs at such a high dose in animal experiments. Fifth, plasma KP‐10 concentration in ApoE−/− mice infused with KP‐10 was significantly higher by 3‐ to 4‐fold (Table [URL='https://www.ahajournals.org/doi/10.1161/JAHA.117.005790#jah32173-tbl-0001']1[/URL]), which were not as high as we anticipated. KP‐10 might therefore be metabolized, to some degree, in circulating blood.[URL='https://www.ahajournals.org/doi/10.1161/JAHA.117.005790#jah32173-bib-0043']43[/URL] Last, plasma KP‐10 concentration in ApoE−/− mice infused with KP‐10+P234 was higher compared with KP‐10 alone (Table [URL='https://www.ahajournals.org/doi/10.1161/JAHA.117.005790#jah32173-tbl-0002']2[/URL]). Given that the amino‐acid sequence of KP‐10 is 70% identical to that of P234 (inactive form), the ELISA kit may detect P234 as KP‐10 (possible cross‐reaction).[/I][/INDENT] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
Kisspeptin-10 as a replacement for compounded HCG?
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