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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
Testosterone Caused Folliculitis
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<blockquote data-quote="Nelson Vergel" data-source="post: 158032" data-attributes="member: 3"><p>This applies to acne and folliculitis:</p><p></p><p>"Acne is a disorder of the pilosebaceous unit in the face, neck, and upper trunk. It has been known that sebaceous glands are androgen target tissues. Castration could prevent sebum production, while testosterone replacement could reverse this condition [87]. AR has been detected in the epithelial cells of sebaceous glands by immunohistochemistry and biochemical binding assays [18].</p><p></p><p>In addition, sebaceous glands contain most of the steroidogenic enzymes for the conversion of DHEA/DHEAS (DHEA sulfate) into testosterone and DHT [15,32]. There are three isoforms of 5α-reductase, and their expression patterns vary across species and tissues [105]. Type I 5α-reductase mainly express in the sebocytes, keratinocytes, and dermal fibroblasts; type II 5α-reductase is mainly detected in the seminal vesicles, epididymis, prostate, and fibroblasts from adult genital skin, as well as the inner root sheath of the hair follicle; while the newly found type III 5α-reductase is detected in the prostate cancer and sebocyte cell lines [17,93]. In addition to its steroidogenic activity, type III 5α-reductase is critically involved in N-linked glycosylation [11]. Intriguingly, the sebum production rate in patients with the deficiency of type II 5α-reductase was similar to that of normal males [52], suggesting that DHT produced locally by type I 5α-reductase enhances sebum production. However in the clinical and in vitro studies, selective inhibitors for type I 5α-reductase did not significantly reduce sebum production and improve acne vulgaris [62,97], indicating that suppression of 5α-reductase alone might not be sufficient to improve acne. There are several possibilities to explain this. First, suppression of an individual type of 5α-reductase might not be sufficient to completely block DHT synthesis due to the redundancy between different types of 5α-reductase, and the sebaceous glands might be sensitive to even tiny amounts of DHT. Second, the newly found type III 5α-reductase might play a more important role in regulating sebum production. Third, in addition to the difference in their potency, testosterone and DHT do not act the same way on AR activation [36], suggesting that testosterone, rather than DHT, could be a more important regulator in sebum production. Additionally, the participation of AR coregulators might compensate for the deficit in DHT production."</p><p></p><p>From: <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3763909/" target="_blank">The Role of Androgen and Androgen Receptor in the Skin-Related Disorders</a></p></blockquote><p></p>
[QUOTE="Nelson Vergel, post: 158032, member: 3"] This applies to acne and folliculitis: "Acne is a disorder of the pilosebaceous unit in the face, neck, and upper trunk. It has been known that sebaceous glands are androgen target tissues. Castration could prevent sebum production, while testosterone replacement could reverse this condition [87]. AR has been detected in the epithelial cells of sebaceous glands by immunohistochemistry and biochemical binding assays [18]. In addition, sebaceous glands contain most of the steroidogenic enzymes for the conversion of DHEA/DHEAS (DHEA sulfate) into testosterone and DHT [15,32]. There are three isoforms of 5α-reductase, and their expression patterns vary across species and tissues [105]. Type I 5α-reductase mainly express in the sebocytes, keratinocytes, and dermal fibroblasts; type II 5α-reductase is mainly detected in the seminal vesicles, epididymis, prostate, and fibroblasts from adult genital skin, as well as the inner root sheath of the hair follicle; while the newly found type III 5α-reductase is detected in the prostate cancer and sebocyte cell lines [17,93]. In addition to its steroidogenic activity, type III 5α-reductase is critically involved in N-linked glycosylation [11]. Intriguingly, the sebum production rate in patients with the deficiency of type II 5α-reductase was similar to that of normal males [52], suggesting that DHT produced locally by type I 5α-reductase enhances sebum production. However in the clinical and in vitro studies, selective inhibitors for type I 5α-reductase did not significantly reduce sebum production and improve acne vulgaris [62,97], indicating that suppression of 5α-reductase alone might not be sufficient to improve acne. There are several possibilities to explain this. First, suppression of an individual type of 5α-reductase might not be sufficient to completely block DHT synthesis due to the redundancy between different types of 5α-reductase, and the sebaceous glands might be sensitive to even tiny amounts of DHT. Second, the newly found type III 5α-reductase might play a more important role in regulating sebum production. Third, in addition to the difference in their potency, testosterone and DHT do not act the same way on AR activation [36], suggesting that testosterone, rather than DHT, could be a more important regulator in sebum production. Additionally, the participation of AR coregulators might compensate for the deficit in DHT production." From: [URL="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3763909/"]The Role of Androgen and Androgen Receptor in the Skin-Related Disorders[/URL] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
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Testosterone Caused Folliculitis
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