View source for Androgen

{{Short description|Any steroid hormone that promotes male characteristics}}
{{About|androgens as natural hormones|androgens as medications|Anabolic steroid|and|Androgen replacement therapy}}
{{Redirect|Androgenic|articles related to adrenaline (epinephrine) or noradrenaline (norepinephrine)|Adrenergic}}
{{Use dmy dates|date=February 2023}}
{{cs1 config|name-list-style=vanc}}
{{Infobox drug class
| Image = Testosteron.svg
| ImageClass = skin-invert-image
| Alt =
| Caption = Testosterone, the major androgen
| Width = 225px
| Synonyms = Androgenic hormone; Testoid
| Use = [[Hypogonadism]], [[transgender men]], [[performance enhancement]], [[bodybuilding]], others
| MeshID = D000728
| Consumer_Reports =
| ATC_prefix = G03B
| Drugs.com =
| Biological_target = [[Androgen receptor]], [[Membrane androgen receptor|mAR]]s (e.g., [[GPRC6A]], others)
}}
An '''androgen''' (from Greek ''andr-'', the stem of the word meaning {{gloss|man}}) is any natural or synthetic [[steroid hormone]] that regulates the development and maintenance of male characteristics in [[vertebrate]]s by binding to [[androgen receptor]]s.<ref name="Moini">{{Cite book| vauthors = Moini J |quote=Androgen is the generic term for any natural or synthetic compound, usually a steroid hormone, which stimulates or controls the development of masculine characteristics by binding to androgen receptors.|title=Fundamental Pharmacology for Pharmacy Technicians|date=2015|publisher=Cengage Learning|isbn=978-1-30-568615-1|page=338|url=https://books.google.com/books?id=P7vyBgAAQBAJ&pg=PA338}}</ref><ref name="Gylys">{{Cite book| vauthors = Gylys BA, Wedding ME |quote=Generic term for an agent (usually a hormone, such as testosterone or androsterone) that stimulates development of male characteristics.|title=Medical Terminology Systems: A Body Systems Approach|date=2017|publisher=F.A. Davis|isbn=978-0-80-365868-4|page=82|url=https://books.google.com/books?id=wMttDgAAQBAJ&pg=PA82}}</ref> This includes the embryological development of the primary [[male sex organs]], and the development of male [[secondary sex characteristic]]s at [[puberty]]. Androgens are synthesized in the [[testes]], the [[ovaries]], and the [[adrenal glands]].

Androgens increase in both males and females during puberty.<ref>{{cite web | url=http://www.fasthealthfitness.com/get-rid-of-pimples/ | title = 15 Ways To Get Rid of Pimples Overnight Natural | publisher=Fast Health Fitness | date = 2016-05-17 }}</ref> The major androgen in males is [[testosterone]].<ref name="Carlson 326">{{cite book | vauthors = Carlson N | title = Physiology of Behavior | publisher = Pearson | series = Reproductive Behavior | volume = 11th edition | date = 22 January 2012 | pages = 326 | isbn = 978-0205239399}}</ref> [[Dihydrotestosterone]] (DHT) and [[androstenedione]] are of equal importance in male development.<ref name="Carlson 326"/> DHT ''in utero'' causes differentiation of the penis, scrotum and prostate. In adulthood, DHT contributes to balding, prostate growth, and [[sebaceous gland]] activity.

Although androgens are commonly thought of only as male [[Sex steroids|sex hormones]], females also have them, but at lower levels: they function in [[libido]] and [[sexual arousal]]. Androgens are the precursors to [[estrogen]]s in both men and women.

In addition to their role as natural hormones, androgens are used as [[medication]]s; for information on androgens as medications, see the [[androgen replacement therapy]] and [[anabolic steroid]] articles.

{{TOC limit|3}}

==Types and examples==
The main subset of androgens, known as adrenal androgens, is composed of 19-carbon steroids synthesized in the [[zona reticularis]], the innermost layer of the [[adrenal cortex]]. Adrenal androgens function as weak steroids (though some are precursors), and the subset includes [[dehydroepiandrosterone]] (DHEA), [[dehydroepiandrosterone sulfate]] (DHEA-S), [[androstenedione]] (A4), and [[androstenediol]] (A5).

Besides testosterone, other androgens include:
* Dehydroepiandrosterone (DHEA) is a steroid hormone produced in the adrenal cortex from [[cholesterol]].<ref>{{cite web | url=http://www.diasource-diagnostics.com/en/Products/ImmunoAssays/Fertility/Androgens | title=Androgens | publisher=DIAsource | access-date=26 June 2013 | archive-date=8 August 2014 | archive-url=https://web.archive.org/web/20140808035826/http://www.diasource-diagnostics.com/en/Products/ImmunoAssays/Fertility/Androgens | url-status=dead }}</ref> It is the primary precursor of both the androgen and [[estrogen]] sex hormones. DHEA is also called dehydroisoandrosterone or dehydroandrosterone.
* Androstenedione (A4) is an androgenic steroid produced by the [[testes]], adrenal cortex, and [[ovaries]]. While androstenedione is converted metabolically to [[testosterone]] and other androgens, it is also the parent structure of [[estrone]]. Use of androstenedione as an athletic or [[bodybuilding supplement]] has been banned by the [[International Olympic Committee]], as well as other sporting organizations.
* [[Androstenediol]] (A5) is a steroid [[metabolite]] of DHEA and the precursor to sex hormones [[testosterone]] and [[estradiol]].
* [[Androsterone]] is a chemical byproduct created during the breakdown of androgens, or derived from [[progesterone]], that also exerts minor masculinising effects, but with one-seventh the intensity of testosterone.  It is found in approximately equal amounts in the [[blood plasma|plasma]] and [[urine]] of both males and females.
* [[Dihydrotestosterone]] (DHT) is a metabolite of testosterone, and a more potent androgen than testosterone in that it binds more strongly to androgen receptors. It is produced in the skin and reproductive tissue.
* A4 and testosterone can also have an extra hydroxyl (-OH) or ketone (=O) group bound on position 11. In this case you can have [[11-hydroxyandrostenedione]], [[11-ketoandrostenedione]], [[11-hydroxytestosterone]], and [[11-ketotestosterone]]. The latter has the same biological activity as testosterone<ref name = "Adriaansen_2024">{{cite journal | vauthors = Adriaansen BP, Oude Alink SE, Swinkels DW, Schröder MA, Span PN, Sweep FC, Claahsen-van der Grinten HL, van Herwaarden AE | display-authors = 6 | title = Reference intervals for serum 11-oxygenated androgens in children | journal = European Journal of Endocrinology | volume = 190 | issue = 1 | pages = 96–103 | date = January 2024 | pmid = 38243909 | doi = 10.1093/ejendo/lvae008 | doi-access = free | url = https://repository.ubn.ru.nl//bitstream/handle/2066/303614/303614.pdf }}</ref> and, therefore, these are also very important in healthy individuals and patients with diseases like, congenital adrenal hyperplasia, polycystic ovarian syndrome, or premature adrenarche.<ref name = "Adriaansen_2024" /> 

Determined by consideration of all biological assay methods ({{circa|1970}}):<ref name="BriggsBrotherton">{{cite book |last1=Briggs MH, Brotherton J |title=Steroid Biochemistry and Pharmacology |date=3 February 1970 |publisher=Academic Press |location=London |isbn=978-0-12-134650-8}}</ref>

=== Female ovarian and adrenal androgens ===

The ovaries and adrenal glands also produce androgens, but at much lower levels than the testes. Regarding the relative contributions of ovaries and adrenal glands to female androgen levels, in a study with six menstruating women the following observations have been made:<ref name="1974 Abraham Ovarian Adrenal Androgens">{{cite journal | vauthors = Abraham GE | title = Ovarian and adrenal contribution to peripheral androgens during the menstrual cycle | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 39 | issue = 2 | pages = 340–346 | date = August 1974 | pmid = 4278727 | doi = 10.1210/jcem-39-2-340 }}</ref>
* Adrenal contribution to peripheral T, DHT, A, DHEA and DHEA-S is relatively constant throughout the [[menstrual cycle]].
* Ovarian contribution of peripheral T, A and DHEA-S reaches maximum levels at mid-cycle, whereas ovarian contribution to peripheral DHT and DHEA does not seem to be influenced by the menstrual cycle.
* Ovary and adrenal cortex contribute equally to peripheral T, DHT and A, with the exception that at mid-cycle ovarian contribution of peripheral A is twice that of the adrenal.
* Peripheral DHEA and DHEA-S are produced mainly in the adrenal cortex which provides 80% of DHEA and over 90% of DHEA-S.

{| class="wikitable"
|+ Ovarian and adrenal contribution to peripheral androgens during the menstrual cycle<ref name="1974 Abraham Ovarian Adrenal Androgens"/>
! Androgen || '''Ovarian (%) (F, M, L)''' || '''Adrenal (%)'''
|-
| DHEA || 20 || 80
|-
| DHEA-S || 4, 10, 4 || 90–96
|-
| Androstenedione || 45, 70, 60 || 30–55
|-
| Testosterone || 33, 60, 33 || 40–66
|-
| DHT || 50 || 50
|-
| colspan="3" | F = early follicular, M = midcycle, L = late luteal phase.
|}

==Biological function==

===Male prenatal development===

====Testes formation====
During mammalian development, the gonads are at first capable of becoming either [[ovary|ovaries]] or testes.<ref>{{Cite book  |year=2000 |title=Developmental Biology |publisher=[[Sinauer Associates]] |location=[[Sunderland, Massachusetts]] |edition=6th |isbn=978-0-87893-243-6 |url=https://archive.org/details/developmentalbio00gilb | vauthors = Gilbert SF |url-access=registration }}{{Page needed|date=September 2010}}</ref> In humans, starting at about week 4, the gonadal rudiments are present within the [[intermediate mesoderm]] adjacent to the developing kidneys. At about week 6, epithelial [[sex cords]] develop within the forming testes and incorporate the [[germ cell]]s as they migrate into the gonads. In males, certain [[Y chromosome]] genes, particularly [[SRY]], control development of the male phenotype, including conversion of the early bipotential gonad into testes. In males, the sex cords fully invade the developing gonads.

====Androgen production====
The mesoderm-derived [[Epithelium|epithelial]] cells of the sex cords in developing testes become the [[Sertoli cell]]s, which will function to support sperm cell formation. A minor population of nonepithelial cells appear between the tubules by week 8 of human fetal development. These are [[Leydig cell]]s. Soon after they differentiate, Leydig cells begin to produce androgens.

====Androgen effects====
The androgens function as [[Paracrine signalling|paracrine]] [[hormone]]s required by the Sertoli cells to support sperm production. They are also required for the masculinization of the developing male fetus (including penis and scrotum formation). Under the influence of androgens, remnants of the [[mesonephron]], the [[Wolffian ducts]], develop into the [[epididymis]], [[vas deferens]] and [[seminal vesicles]]. This action of androgens is supported by a hormone from Sertoli cells, Müllerian inhibitory hormone (MIH), which prevents the embryonic Müllerian ducts from developing into fallopian tubes and other female reproductive tract tissues in male embryos. MIH and androgens cooperate to allow for movement of testes into the scrotum.

====Early regulation====
Before the production of the pituitary hormone [[luteinizing hormone]] (LH) by the embryo starting at about weeks 11–12, [[human chorionic gonadotrophin]] (hCG) promotes the differentiation of Leydig cells and their production of androgens at week 8.  Androgen action in target tissues often involves conversion of testosterone to 5α-[[dihydrotestosterone]] (DHT).

===Male pubertal development===
At the time of [[puberty]], androgen levels increase dramatically in males, and androgens mediate the development of masculine [[secondary sexual characteristic]]s as well as the activation of [[spermatogenesis]] and [[fertility]] and masculine behavioral changes such as increased [[sex drive]]. Masculine secondary sexual characteristics include [[androgenic hair]], [[voice deepening]], emergence of the [[Adam's apple]], broadening of the shoulders, increased [[muscle mass]], and [[penile growth]].

===Spermatogenesis===
During puberty, androgen, LH and [[follicle stimulating hormone]] (FSH) production increase and the sex cords hollow out, forming the seminiferous tubules, and the germ cells start to differentiate into sperm. Throughout adulthood, androgens and FSH cooperatively act on Sertoli cells in the testes to support sperm production.<ref>{{Cite book|editor1=Saffron A. Whitehead |editor2=Stephen Nussey |title=Endocrinology: an integrated approach |publisher=[[British Institute of Organ Studies]] |location=Oxford |year=2001 |isbn=978-1-85996-252-7 |url=https://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=endocrin |author1=Stephen Nussey |author2=Saffron Whitehead }}{{Page needed|date=September 2010}}</ref> Exogenous androgen supplements can be used as a [[male contraceptive]]. Elevated androgen levels caused by use of androgen supplements can inhibit production of LH and block production of endogenous androgens by Leydig cells. Without the locally high levels of androgens in testes due to androgen production by Leydig cells, the seminiferous tubules can degenerate, resulting in infertility. For this reason, many transdermal androgen patches are applied to the scrotum.

===Fat deposition===
Males typically have less body fat than females. Recent results indicate androgens inhibit the ability of some fat cells to store lipids by blocking a signal transduction pathway that normally supports adipocyte function.<ref name="Singh R, Artaza JN, Taylor WE, et al. 2006 141–54">{{cite journal | vauthors = Singh R, Artaza JN, Taylor WE, Braga M, Yuan X, Gonzalez-Cadavid NF, Bhasin S | title = Testosterone inhibits adipogenic differentiation in 3T3-L1 cells: nuclear translocation of androgen receptor complex with beta-catenin and T-cell factor 4 may bypass canonical Wnt signaling to down-regulate adipogenic transcription factors | journal = Endocrinology | volume = 147 | issue = 1 | pages = 141–154 | date = January 2006 | pmid = 16210377 | pmc = 4417624 | doi = 10.1210/en.2004-1649 }}</ref> Also, androgens, but not estrogens, increase beta [[adrenergic receptor]]s while decreasing alpha adrenergic receptors—which results in increased levels of epinephrine/norepinephrine due to lack of alpha-2 receptor negative feedback and decreased fat accumulation due to epinephrine/norepinephrine then acting on lipolysis-inducing beta receptors.

===Muscle mass===
Males typically have more [[skeletal muscle]] mass than females. Androgens promote the enlargement of skeletal muscle cells in a coordinated manner by acting on several cell types in skeletal muscle tissue.<ref>{{cite journal | vauthors = Sinha-Hikim I, Taylor WE, Gonzalez-Cadavid NF, Zheng W, Bhasin S | title = Androgen receptor in human skeletal muscle and cultured muscle satellite cells: up-regulation by androgen treatment | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 89 | issue = 10 | pages = 5245–5255 | date = October 2004 | pmid = 15472231 | doi = 10.1210/jc.2004-0084 | doi-access = free }}</ref> One cell type, called the [[Muscle cell|myoblast]], conveys androgen receptors for generating muscle. Fusion of myoblasts generates [[myotube]]s, in a process linked to androgen receptor levels.<ref name="pmid15623502">{{cite journal | vauthors = Vlahopoulos S, Zimmer WE, Jenster G, Belaguli NS, Balk SP, Brinkmann AO, Lanz RB, Zoumpourlis VC, Schwartz RJ | display-authors = 6 | title = Recruitment of the androgen receptor via serum response factor facilitates expression of a myogenic gene | journal = The Journal of Biological Chemistry | volume = 280 | issue = 9 | pages = 7786–7792 | date = March 2005 | pmid = 15623502 | doi = 10.1074/jbc.M413992200 | doi-access = free }}</ref> Higher androgen levels lead to increased expression of [[androgen receptor]].

===Brain===
Circulating levels of androgens can influence human behavior because some [[neuron]]s are sensitive to steroid hormones. Androgen levels have been implicated in the regulation of human [[aggression]] and libido. Indeed, androgens are capable of altering the structure of the brain in several species, including mice, rats, and primates, producing [[sex differences]].<ref>{{cite journal | vauthors = Cooke B, Hegstrom CD, Villeneuve LS, Breedlove SM | title = Sexual differentiation of the vertebrate brain: principles and mechanisms | journal = Frontiers in Neuroendocrinology | volume = 19 | issue = 4 | pages = 323–362 | date = October 1998 | pmid = 9799588 | doi = 10.1006/frne.1998.0171 | s2cid = 14372914 }}</ref> More recent studies showing the general [[Mood (psychology)|mood]] of [[transgender men]], who have undergone [[transgender hormone replacement therapy]] replacing [[estrogen]]s with androgens, do not show any substantial long-term [[behavioral]] changes.<ref>{{cite journal | vauthors = Irwig MS | title = Testosterone therapy for transgender men | journal = The Lancet. Diabetes & Endocrinology | volume = 5 | issue = 4 | pages = 301–311 | date = April 2017 | pmid = 27084565 | doi = 10.1016/S2213-8587(16)00036-X }}</ref><ref>{{cite journal | vauthors = Costantino A, Cerpolini S, Alvisi S, Morselli PG, Venturoli S, Meriggiola MC | title = A prospective study on sexual function and mood in female-to-male transsexuals during testosterone administration and after sex reassignment surgery | journal = Journal of Sex & Marital Therapy | volume = 39 | issue = 4 | pages = 321–335 | date = 14 February 2013 | pmid = 23470169 | doi = 10.1080/0092623X.2012.736920 | s2cid = 34943756 }}</ref><ref>{{cite journal | vauthors = Johnson JM, Nachtigall LB, Stern TA | title = The effect of testosterone levels on mood in men: a review | journal = Psychosomatics | volume = 54 | issue = 6 | pages = 509–514 | date = 1 November 2013 | pmid = 24016385 | doi = 10.1016/j.psym.2013.06.018 }}</ref>

Numerous reports have shown androgens alone are capable of altering the [[structure of the brain]],<ref>{{cite journal | vauthors = Zuloaga DG, Puts DA, Jordan CL, Breedlove SM | title = The role of androgen receptors in the masculinization of brain and behavior: what we've learned from the testicular feminization mutation | journal = Hormones and Behavior | volume = 53 | issue = 5 | pages = 613–626 | date = May 2008 | pmid = 18374335 | pmc = 2706155 | doi = 10.1016/j.yhbeh.2008.01.013 }}</ref> but identification of which alterations in neuroanatomy stem from androgens or estrogens is difficult, because of their potential for conversion.

Evidence from [[neurogenesis]] (formation of new neurons) studies on male rats has shown that the [[hippocampus]] is a useful brain region to examine when determining the effects of androgens on behavior. To examine [[neurogenesis]], wild-type male rats were compared with male rats that had [[androgen insensitivity syndrome]], a genetic difference resulting in complete or partial insensitivity to androgens and a lack of external [[male genitalia]].

Neural injections of [[bromodeoxyuridine]] (BrdU) were applied to males of both groups to test for [[neurogenesis]]. Analysis showed that [[testosterone]] and [[dihydrotestosterone]] regulated adult [[Hippocampal formation|hippocampal]] [[neurogenesis]] (AHN). Adult hippocampal neurogenesis was regulated through the [[androgen receptor]] in the wild-type male rats, but not in the TMF male rats. To further test the role of activated androgen receptors on AHN, [[flutamide]], an [[antiandrogen]] drug that competes with testosterone and dihydrotestosterone for androgen receptors, and dihydrotestosterone were administered to normal male rats. Dihydrotestosterone increased the number of BrdU cells, while flutamide inhibited these cells. Moreover, estrogens had no effect. This research demonstrates how androgens can increase AHN.<ref name="pmid23782943">{{cite journal | vauthors = Hamson DK, Wainwright SR, Taylor JR, Jones BA, Watson NV, Galea LA | title = Androgens increase survival of adult-born neurons in the dentate gyrus by an androgen receptor-dependent mechanism in male rats | journal = Endocrinology | volume = 154 | issue = 9 | pages = 3294–3304 | date = September 2013 | pmid = 23782943 | doi = 10.1210/en.2013-1129 | hdl-access = free | doi-access = free | hdl = 2429/63213 }}</ref>

Researchers also examined how mild exercise affected androgen synthesis which in turn causes AHN activation of [[N-Methyl-D-aspartic acid|''N''-methyl-{{sc|D}}-aspartate (NMDA)]] receptors. [[NMDA]] induces a calcium flux that allows for synaptic plasticity which is crucial for AHN.

Researchers injected both orchidectomized (ORX) (castrated) and sham castrated male rats with [[BrdU]] to determine if the number of new cells was increased. They found that AHN in male rats is increased with mild exercise by boosting synthesis of [[dihydrotestosterone]] in the [[hippocampus]]. Again it was noted that AHN was not increased via activation of the [[estrogen receptor]]s.<ref>{{cite journal | vauthors = Okamoto M, Hojo Y, Inoue K, Matsui T, Kawato S, McEwen BS, Soya H | title = Mild exercise increases dihydrotestosterone in hippocampus providing evidence for androgenic mediation of neurogenesis | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 109 | issue = 32 | pages = 13100–13105 | date = August 2012 | pmid = 22807478 | pmc = 3420174 | doi = 10.1073/pnas.1210023109 | doi-access = free | bibcode = 2012PNAS..10913100O }}</ref>

Androgen regulation decreases the likelihood of [[Depression (clinical)|depression]] in males. In [[preadolescent]] male rats, [[neonatal]] rats treated with [[flutamide]] developed more [[Depression symptoms|depression-like symptoms]] compared to control rats.

Again [[BrdU]] was injected into both groups of rats in order to see if cells were multiplying in the living tissue. These results demonstrate how the organization of androgens has a positive effect on [[preadolescent]] [[Hippocampal formation|hippocampal]] [[neurogenesis]] that may be linked with lower [[Depression symptoms|depression-like symptoms]].<ref name="pmid20399256">{{cite journal | vauthors = Zhang JM, Tonelli L, Regenold WT, McCarthy MM | title = Effects of neonatal flutamide treatment on hippocampal neurogenesis and synaptogenesis correlate with depression-like behaviors in preadolescent male rats | journal = Neuroscience | volume = 169 | issue = 1 | pages = 544–554 | date = August 2010 | pmid = 20399256 | pmc = 3574794 | doi = 10.1016/j.neuroscience.2010.03.029 }}</ref>

[[Social isolation]] has a hindering effect in AHN whereas normal regulation of androgens increases AHN. A study using male rats showed that [[testosterone]] may block [[social isolation]], which results in [[Hippocampal formation|hippocampal]] [[neurogenesis]] reaching [[homeostasis]]—regulation that keeps internal conditions stable. A [[BrdU|Brdu]] analysis showed that excess [[testosterone]] did not increase this blocking effect against [[social isolation]]; that is, the natural circulating levels of androgens cancel out the negative effects of [[social isolation]] on AHN.<ref name="pmid21875652">{{cite journal | vauthors = Spritzer MD, Ibler E, Inglis W, Curtis MG | title = Testosterone and social isolation influence adult neurogenesis in the dentate gyrus of male rats | journal = Neuroscience | volume = 195 | pages = 180–190 | date = November 2011 | pmid = 21875652 | pmc = 3198792 | doi = 10.1016/j.neuroscience.2011.08.034 }}</ref>

===Female-specific effects===
Androgens have potential roles in relaxation of the [[myometrium]] via non-genomic, [[androgen receptor]]-independent pathways, preventing premature [[uterine contraction]]s in pregnancy.<ref name="MakievaSaunders2014">{{cite journal | vauthors = Makieva S, Saunders PT, Norman JE | title = Androgens in pregnancy: roles in parturition | journal = Human Reproduction Update | volume = 20 | issue = 4 | pages = 542–559 | year = 2014 | pmid = 24643344 | pmc = 4063701 | doi = 10.1093/humupd/dmu008 }}</ref>

===Androgen insensitivity===
{{Main|Androgen insensitivity syndrome}}
Reduced ability of an [[sex chromosome|XY]]-[[karyotype]] fetus to respond to androgens can result in one of several conditions, including infertility and several forms of [[intersex]] conditions.

===Miscellaneous===
Yolk androgen levels in certain birds have been positively correlated to social dominance later in life. See [[American coot]].

==Biological activity==
Androgens bind to and activate [[androgen receptor]]s (ARs) to mediate most of their [[biological effect]]s.

===Relative potency===
Determined by consideration of all biological assay methods ({{circa|1970}}):<ref name="BriggsBrotherton"/>

{| class="wikitable"
! Androgen !! Potency (%)
|-
| Testosterone || 40
|-
| 5α-Dihydrotestosterone (DHT) || 100
|-
| Androstenediol || .0008
|-
| Androstenedione || .04
|-
| Dehydroepiandrosterone || .02
|-
| Androsterone || .06
|}

5α-Dihydrotestosterone (DHT) was 2.4&nbsp;times more potent than testosterone at maintaining normal prostate weight and duct lumen mass (this is a measure of epithelial cell function stimulation). Whereas DHT was equally potent as testosterone at preventing prostate cell death after castration.<ref name="pmid8958218">{{cite journal | vauthors = Wright AS, Thomas LN, Douglas RC, Lazier CB, Rittmaster RS | title = Relative potency of testosterone and dihydrotestosterone in preventing atrophy and apoptosis in the prostate of the castrated rat | journal = The Journal of Clinical Investigation | volume = 98 | issue = 11 | pages = 2558–2563 | date = December 1996 | pmid = 8958218 | pmc = 507713 | doi = 10.1172/JCI119074 }}</ref>
One of the 11-oxygenated androgens, namely 11-ketotestosterone, has the same potency as testosterone. <ref>{{cite journal | vauthors = Adriaansen BP, Oude Alink SE, Swinkels DW, Schröder MA, Span PN, Sweep FC, Claahsen-van der Grinten HL, van Herwaarden AE | display-authors = 6 | title = Reference intervals for serum 11-oxygenated androgens in children | journal = European Journal of Endocrinology | volume = 190 | issue = 1 | pages = 96–103 | date = January 2024 | pmid = 38243909 | doi = 10.1093/ejendo/lvae008 | doi-access = free | url = https://repository.ubn.ru.nl//bitstream/handle/2066/303614/303614.pdf }}</ref>

===Non-genomic actions===
Androgens have also been found to signal through [[membrane androgen receptor]]s, which are distinct from the classical nuclear androgen receptor.<ref name="pmid19931639">{{cite journal | vauthors = Bennett NC, Gardiner RA, Hooper JD, Johnson DW, Gobe GC | title = Molecular cell biology of androgen receptor signalling | journal = The International Journal of Biochemistry & Cell Biology | volume = 42 | issue = 6 | pages = 813–827 | date = June 2010 | pmid = 19931639 | doi = 10.1016/j.biocel.2009.11.013 }}</ref><ref name="pmid25257522">{{cite journal | vauthors = Wang C, Liu Y, Cao JM | title = G protein-coupled receptors: extranuclear mediators for the non-genomic actions of steroids | journal = International Journal of Molecular Sciences | volume = 15 | issue = 9 | pages = 15412–15425 | date = September 2014 | pmid = 25257522 | pmc = 4200746 | doi = 10.3390/ijms150915412 | doi-access = free }}</ref><ref name="pmid23746222">{{cite journal | vauthors = Lang F, Alevizopoulos K, Stournaras C | title = Targeting membrane androgen receptors in tumors | journal = Expert Opinion on Therapeutic Targets | volume = 17 | issue = 8 | pages = 951–963 | date = August 2013 | pmid = 23746222 | doi = 10.1517/14728222.2013.806491 | s2cid = 23918273 }}</ref>

==Biochemistry==
[[File:Steroidogenesis.svg|thumb|450px|class=skin-invert-image|[[Steroidogenesis]], showing the relation between several androgens, is at bottom left. Estrone and estradiol, in contrast, are [[estrogens]].]]

===Biosynthesis===
Androgens are [[biosynthesis|synthesized]] from [[cholesterol]] and are produced primarily in the [[gonad]]s (testicles and ovaries) and also in the [[adrenal gland]]s. The testicles produce a much higher quantity than the ovaries. Conversion of testosterone to the more potent DHT occurs in [[prostate gland]], [[liver]], [[brain]] and skin.

{{Production rates, secretion rates, clearance rates, and blood levels of major sex hormones}}

===Metabolism===
Androgens are [[metabolism|metabolized]] mainly in the [[liver]].

==Medical uses==
{{Main|Anabolic steroid#Medical}}

A low testosterone level (hypogonadism) in men may be treated with testosterone administration. Prostate cancer may be treated by removing the major source of testosterone: testicle removal ([[orchiectomy]]); or agents which block androgens from accessing their receptor: [[antiandrogen]]s.

== See also ==
{{Col div|colwidth=40em}}
* [[Androgen insensitivity syndrome]]
* [[Androgen insufficiency syndrome]]
* [[Andrology]]
* [[Endocrine system]]
* [[Exercise and androgen levels]]
* [[List of androgens/anabolic steroids]]
* [[List of androgens/anabolic steroids available in the United States]]
* [[List of steroid abbreviations]]
* [[Testosterone and the cardiovascular system]]
{{Colend}}

== References ==
{{Reflist}}

{{Androgens and antiandrogens}}
{{Androgen receptor modulators}}
{{Endogenous steroids}}
{{Authority control}}

[[Category:Anabolic–androgenic steroids| ]]
[[Category:Hepatotoxins]]
[[Category:Hormones of the hypothalamus-pituitary-gonad axis]]
[[Category:Sex hormones]]