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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
What is the Function of Sex Hormone Binding Globulin SHBG?
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<blockquote data-quote="Nelson Vergel" data-source="post: 178221" data-attributes="member: 3"><p>Sex hormone-binding globulin (SHBG) is a serum glycoprotein exhibiting the unique feature of binding sex steroids with high affinity and specificity. Its serum levels are regulated not only by androgens and estrogens but also by thyroid hormones and other metabolic factors. Several disease conditions are accompanied by altered SHBG levels such as hyper- and hypoandrogenism, thyroid disorders, pituitary diseases, liver disorders, and breast as well as prostate cancer. Additionally, several drugs and alcohol consumption influence serum concentrations of SHBG. In some cases, altered SHBG levels are a specific result of the underlying pathology. In others, they merely constitute an epiphenomenon, which still might offer the possibility of using serum measurements of SHBG as surrogate marker. This review article portrays the different disorders associated with altered SHBG levels and discusses the usefulness of SHBG as disease biomarker from a clinicians as well as from an endocrinological researchers point of view.</p><p></p><p><strong><span style="font-size: 18px">SHBG and exogenous administered drugs, xenobiotics and alcohol</span></strong></p><p></p><p>Numerous drugs influence SHBG serum levels via variation of its hepatic synthesis rate. SHBG synthesis is e as already mentioned above e modulated by sex steroids. Application of estrogenic, progestogenic and androgenic compounds will therefore result in altered SHBG concentrations.</p><p></p><p>Estrogens cause considerable increases in SHBG levels. The extent is dependent on the route of administration: oral formulations will cause more pronounced effects than transdermal ones as the active component directly accesses the portal system and the liver will be exposed to very high concentrations [10,12,68]. With application of tamoxifen, raloxifene and clomiphene SHBG levels have been observed in both sexes. Hence, selective estrogen receptor modulators generally seem to exhibit agonistic characteristics with respect to SHBG synthesis [12,69]. As well, SHBG elevations in adrenal carcinoma patients treated with mitotane are attributed to the drug's agonistic effects on hepatic estrogen receptors [70]. Progestins on the other hand have been known for a long time to significantly decrease SHBG serum levels [71]. Consequently, SHBG levels in women receiving combination oral contraceptives (COC) depend on the proportion of the contained estrogen and progestin [72]. Application of androgens in male hypogonadism as well as suppression of pituitary gonadotropin release with the testosterone derivative danazol causes</p><p></p><p>SHBG concentrations to decrease [12,73,74]. A drop of SHBG levels has also been described with the use of the antiandrogen cyproterone acetate. The observation is attributed to its progestogenic properties but might also be due to partly agonistic effects in the liver [12]. Beyond sex steroids,treatment with synthetic glucocorticoids has been associated with decreasing SHBG levels. Findings,however, are inconsistent across different studies and results of in vitro experiments are ambiguous [13].</p><p> </p><p>Another class of drugs influencing SHBG levels are hepatic enzyme inducers like phenobarbital, phenytoin, carbamazepine or rifampicin, which regularly result in elevated SHBG concentrations [10].</p><p></p><p>The effect has been best investigated in liver enzyme inducing antiepileptic drugs (LEIAED). Increased SHBG concentrations in men on LEIAED therapy contribute to the common hormonal and reproductive disturbances in these patients [75]. In women, LEIAED associated SHBG increase might cause failure of COC by tightly binding progestins and lowering free progestin levels.</p><p></p><p>Finally, SHBG and drugs are not only interconnected via hepatic synthesis but also by plasma steroid transport. Drugs might exert their effects and side effects by occupying SHBG binding sites and displacing the natural ligands. Furthermore, SHBG has been implied in the transport of xenobiotic ligands in plasma and across cell membranes [13]. Both topics, however, require further research to enable proper judgment of relevance.</p><p></p><p>Moderate alcohol consumption is associated with slightly but significantly decreased SHBG levels in both sexes in the majority of studies [76,77]. In e non-cirrhotic e alcoholics, however, approximately 3-fold increased SHBG-levels have been described, which might contribute to the hypogonadism often observed in these patients [78]. Beyond that, chronic alcohol ingestion also impairs glycosylation during protein synthesis resulting in SHBG isoforms with altered carbohydrate composition. Withdrawal causes SHBG levels to decrease promptly, but values within reference ranges are only reached after several weeks of abstinence [78].</p><p></p><p>Awareness of the relation of drugs and SHBG levels helps to explain some effects and side effects of therapy. When not explicitly evaluating gonadal and sexual dysfunction, however, there is no need to determine SHBG in day-to-day routine in patients receiving the respective medication. The connections of SHBG and xenobiotics require more detailed investigations and might constitute a rewarding research area.</p><p></p><p>Reference: <a href="https://www.sciencedirect.com/science/article/abs/pii/S1521690X15000664" target="_blank">The biomarker sex hormone-binding globulin – From established applications to emerging trends in clinical medicine</a></p></blockquote><p></p>
[QUOTE="Nelson Vergel, post: 178221, member: 3"] Sex hormone-binding globulin (SHBG) is a serum glycoprotein exhibiting the unique feature of binding sex steroids with high affinity and specificity. Its serum levels are regulated not only by androgens and estrogens but also by thyroid hormones and other metabolic factors. Several disease conditions are accompanied by altered SHBG levels such as hyper- and hypoandrogenism, thyroid disorders, pituitary diseases, liver disorders, and breast as well as prostate cancer. Additionally, several drugs and alcohol consumption influence serum concentrations of SHBG. In some cases, altered SHBG levels are a specific result of the underlying pathology. In others, they merely constitute an epiphenomenon, which still might offer the possibility of using serum measurements of SHBG as surrogate marker. This review article portrays the different disorders associated with altered SHBG levels and discusses the usefulness of SHBG as disease biomarker from a clinicians as well as from an endocrinological researchers point of view. [B][SIZE=18px]SHBG and exogenous administered drugs, xenobiotics and alcohol[/SIZE][/B] Numerous drugs influence SHBG serum levels via variation of its hepatic synthesis rate. SHBG synthesis is e as already mentioned above e modulated by sex steroids. Application of estrogenic, progestogenic and androgenic compounds will therefore result in altered SHBG concentrations. Estrogens cause considerable increases in SHBG levels. The extent is dependent on the route of administration: oral formulations will cause more pronounced effects than transdermal ones as the active component directly accesses the portal system and the liver will be exposed to very high concentrations [10,12,68]. With application of tamoxifen, raloxifene and clomiphene SHBG levels have been observed in both sexes. Hence, selective estrogen receptor modulators generally seem to exhibit agonistic characteristics with respect to SHBG synthesis [12,69]. As well, SHBG elevations in adrenal carcinoma patients treated with mitotane are attributed to the drug's agonistic effects on hepatic estrogen receptors [70]. Progestins on the other hand have been known for a long time to significantly decrease SHBG serum levels [71]. Consequently, SHBG levels in women receiving combination oral contraceptives (COC) depend on the proportion of the contained estrogen and progestin [72]. Application of androgens in male hypogonadism as well as suppression of pituitary gonadotropin release with the testosterone derivative danazol causes SHBG concentrations to decrease [12,73,74]. A drop of SHBG levels has also been described with the use of the antiandrogen cyproterone acetate. The observation is attributed to its progestogenic properties but might also be due to partly agonistic effects in the liver [12]. Beyond sex steroids,treatment with synthetic glucocorticoids has been associated with decreasing SHBG levels. Findings,however, are inconsistent across different studies and results of in vitro experiments are ambiguous [13]. Another class of drugs influencing SHBG levels are hepatic enzyme inducers like phenobarbital, phenytoin, carbamazepine or rifampicin, which regularly result in elevated SHBG concentrations [10]. The effect has been best investigated in liver enzyme inducing antiepileptic drugs (LEIAED). Increased SHBG concentrations in men on LEIAED therapy contribute to the common hormonal and reproductive disturbances in these patients [75]. In women, LEIAED associated SHBG increase might cause failure of COC by tightly binding progestins and lowering free progestin levels. Finally, SHBG and drugs are not only interconnected via hepatic synthesis but also by plasma steroid transport. Drugs might exert their effects and side effects by occupying SHBG binding sites and displacing the natural ligands. Furthermore, SHBG has been implied in the transport of xenobiotic ligands in plasma and across cell membranes [13]. Both topics, however, require further research to enable proper judgment of relevance. Moderate alcohol consumption is associated with slightly but significantly decreased SHBG levels in both sexes in the majority of studies [76,77]. In e non-cirrhotic e alcoholics, however, approximately 3-fold increased SHBG-levels have been described, which might contribute to the hypogonadism often observed in these patients [78]. Beyond that, chronic alcohol ingestion also impairs glycosylation during protein synthesis resulting in SHBG isoforms with altered carbohydrate composition. Withdrawal causes SHBG levels to decrease promptly, but values within reference ranges are only reached after several weeks of abstinence [78]. Awareness of the relation of drugs and SHBG levels helps to explain some effects and side effects of therapy. When not explicitly evaluating gonadal and sexual dysfunction, however, there is no need to determine SHBG in day-to-day routine in patients receiving the respective medication. The connections of SHBG and xenobiotics require more detailed investigations and might constitute a rewarding research area. Reference: [URL="https://www.sciencedirect.com/science/article/abs/pii/S1521690X15000664"]The biomarker sex hormone-binding globulin – From established applications to emerging trends in clinical medicine[/URL] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
What is the Function of Sex Hormone Binding Globulin SHBG?
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