It is the hormone that causes the emergence of male secondary characters.
An androgen (from the Greek and-, the root of the word meaning “man”) is any natural or synthetic steroid hormone that regulates the development and maintenance of male characteristics in vertebrates by binding to androgen receptors.
This includes the embryological development of the primary male sex organs and the development of male secondary sex characteristics at puberty. Androgens are synthesized in the testes, ovaries, and adrenal glands.
Androgens increase in both boys and girls during puberty. The primary androgen in men is testosterone. Dihydrotestosterone and androstenedione are equally crucial in male development.
Dihydrotestosterone is the uterus that causes differentiation of the penis, scrotum, and prostate. In adulthood, dihydrotestosterone contributes to baldness, prostate growth, and the activity of the sebaceous glands.
Although androgens are commonly thought to be only male sex hormones, women also have them at lower levels: they function with libido and sexual arousal.
In addition, androgens are the precursors of estrogens in both men and women.
In addition to their role as natural hormones, androgens are used as medicines.
Types and examples
The significant subset of androgens, known as adrenal androgens, is composed of 19-carbon steroids synthesized in the reticular zone, the innermost layer of the adrenal cortex.
Adrenal androgens function as weak steroids (although some are precursors), and the subset includes dehydroepiandrosterone, dehydroepiandrosterone sulfate, androstenedione, and androstenediol.
In addition to testosterone, other androgens include:
Dehydroepiandrosterone is a steroid hormone produced in the adrenal cortex by cholesterol. Dehydroepiandrosterone is also called dehydroisoandrosterone or dehydroandrosterone.
Androsterone is a chemical byproduct created during the breakdown of androgens, or a derivative of progesterone, which also exerts minor effects of masculinization, but with one-seventh of the intensity testosterone.
It is found in approximately equal amounts in the plasma and urine of men and women.
Dihydrotestosterone is a metabolite of testosterone and a more potent androgen than testosterone because it binds more strongly to androgen receptors. It occurs in the skin and the reproductive tissue.
Male prenatal development
During the development of mammals, the gonads are able at first to become ovaries or testes.
In humans, beginning around week 4, the gonadal rudiments are present in the intermediate mesoderm adjacent to the developing kidneys.
Around week 6, the epithelial sex cords develop within the forming testes and incorporate the germ cells as they migrate to the gonads.
In men, specific genes of the Y chromosome, particularly the Y protein of the sex-determining region, control the development of the male phenotype, including the conversion of the early bipotential gonad into testes.
In men, the sexual cords invade the developing gonads entirely.
The epithelial cells derived from the mesoderm of the sexual cords in the developing testes are converted into Sertoli cells, which will function to support the formation of sperm cells.
A smaller population of non-epithelial cells appears between the tubules in week 8 of human fetal development.
These are Leydig cells. Shortly after they differentiate, Leydig cells begin to produce androgens.
Effects of androgens
Androgens function as paracrine hormones required by Sertoli cells to support sperm production. They are also necessary for the masculinization of the developing male fetus (including the formation of the penis and scrotum).
Under the influence of androgens, the remains of the mesonephros, the Wolffian ducts, become the epididymis, the vas deferens, and the seminal vesicles.
This action of androgens is supported by a Sertoli cell hormone, the Müller inhibitory hormone, which prevents the embryonic Müllerian ducts from becoming fallopian tubes and other tissues of the female reproductive system in male embryos.
The inhibitory hormone of Müller and the androgens cooperate to allow the movement of the testes in the scrotum.
Before the production of the luteinizing hormone of the pituitary hormone (LH) by the embryo from approximately weeks 11-12, human chorionic gonadotropin promotes the differentiation of Leydig cells and their androgen production at week 8.
The action of androgens in the target tissues often involves the conversion of testosterone to 5α-dihydrotestosterone.
Male pubertal development
At puberty, androgen levels increase dramatically in men, and androgens mediate the development of male secondary sex characteristics.
As well as the activation of spermatogenesis and fertility and male behavioral changes, such as gynecology and increased sexual desire.
The secondary male sexual characteristics include androgenic hair, deepening of the voice, the appearance of Adam’s apple, widening of the shoulders, increase of the muscular mass, and growth of the penis.
During puberty, androgens increase the production of luteinizing hormone and follicle-stimulating hormone. The sexual cords are hollowed out, forming the seminiferous tubules, and the germ cells begin to differentiate into sperm.
During adulthood, androgens and the follicle-stimulating hormone act cooperatively on the Sertoli cells in the testicles to support sperm production.
Exogenous androgen supplements can be used as male contraceptives.
Elevated levels of androgens caused by androgen supplements can inhibit the production of luteinizing hormone and block the production of endogenous androgens by Leydig cells.
Without the locally high levels of androgens in the testes due to the production of androgens by Leydig cells, the seminiferous tubules can degenerate, resulting in infertility.
For this reason, many patches of transdermal androgens are applied to the scrotum.
Men generally have less body fat than women.
Recent results indicate that androgens inhibit the ability of some fat cells to store lipids by blocking a signal transduction pathway that generally supports the function of adipocytes.
In addition, androgens, but not estrogen, increase beta-adrenergic receptors while decreasing alpha-adrenergic receptors.
What results in high levels of epinephrine/norepinephrine due to lack of negative feedback of the alpha-2 receptor and a reduced accumulation of fat due to epinephrine/norepinephrine acting on lipolysis -inducer beta receptors.
Males usually have more skeletal muscle mass than females.
Androgens promote the enlargement of skeletal muscle cells and probably act in a coordinated fashion to function by working on several types of cells in lean muscle tissue.
One type of cell transmits hormonal signals to generate muscle, the myoblast. Higher levels of androgens lead to greater expression of the androgen receptor.
The fusion of myoblasts generates myotubes in a process related to the levels of the androgen receptor.
Circulating levels of androgens can influence human behavior because some neurons are sensitive to steroid hormones. Androgen levels have been implicated in the regulation of human aggression and libido.
Androgens can alter brain structure in several species, including mice, rats, and primates, producing sex differences.
Numerous reports have shown that androgens alone can alter brain structure, but the identification of alterations in neuroanatomy derived from androgens or estrogens is difficult due to their conversion potential.
Studies of neurogenesis (formation of new neurons) in male rats have shown that the hippocampus is a valuable brain region to examine in determining the effects of androgens on behavior.
To examine neurogenesis, wild-type male rats were compared to male rats with a testicular feminization mutation, a genetic disorder resulting in complete or partial insensitivity to androgens and a lack of external male genitalia.
Neuronal Bromodeoxyuridine injections were applied to men in both groups to evaluate neurogenesis. The analysis showed that testosterone and dihydrotestosterone regulate the neurogenesis of the adult hippocampus.
Neurogenesis of the adult hippocampus was regulated through the androgen receptor in male wild-type rats but not in the mutation of male rats of testicular feminization.
To further test the role of activated androgen receptors in adult hippocampal neurogenesis, flutamide, an antiandrogen drug that competes with testosterone and dihydrotestosterone for androgen receptors dihydrotestosterone, was administered to normal male rats.
Dihydrotestosterone increased the number of bromodeoxyuridine cells, whereas flutamide inhibited these cells.
On the other hand, estrogen had no effect. This research demonstrates how androgens can increase the neurogenesis of the adult hippocampus.
The researchers also examined how mild exercise affected androgen synthesis, which causes the activation of adult hippocampal neurogenesis of N-methyl-D-aspartate receptors.
N-methyl-D-aspartic acid induces a calcium flux that allows synaptic plasticity, crucial for adult hippocampal neurogenesis.
The researchers injected castrated orchidectomized (castrated) male rats and simulated Bromodeoxyuridine to determine whether the number of new cells increased.
They found that adult hippocampal neurogenesis in male rats increases with moderate exercise by increasing the synthesis of dihydrotestosterone in the hippocampus.
Again, it was observed that the neurogenesis of the adult hippocampus did not increase through the activation of the estrogen receptors.
Androgen regulation decreases the likelihood of depression in men. In preadolescent male rats, neonatal rats treated with flutamide developed more symptoms similar to depression than control rats.
Again, Bromodeoxyuridine was injected into both groups of rats to see if the cells were multiplying in the living tissue.
These results demonstrate how the organization of androgens has a positive effect on preadolescent hippocampal neurogenesis that may be related to symptoms similar to depression.
Social isolation has an impeding effect on the neurogenesis of the adult hippocampus, while the normal regulation of androgens increases the neurogenesis of the adult hippocampus.
A study in which male rats were used demonstrated that testosterone could block social isolation, which results in the neurogenesis of the hippocampus reaching the regulation of homeostasis, which keeps internal conditions stable.
An analysis of Bromodeoxyuridine showed that excess testosterone did not increase this blocking effect against social isolation.
The natural circulating levels of androgens cancel the adverse effects of social isolation on the neurogenesis of the adult hippocampus.
Specific effects of women
Androgens have a potential role in the relaxation of the myometrium through non-genomic pathways, independent of androgen receptors, that prevent premature uterine contractions in pregnancy.
Insensitivity to androgens
The reduced ability of an XY-karyotype fetus to respond to androgens can lead to one of several conditions, including infertility and various forms of intersex conditions.
The androgen insensitivity syndrome is an intersexual condition. There is a partial or complete failure of many cells in the affected genetic male to respond to the androgenic hormones.
This can prevent or impair the masculinization of the male genitalia in the development of the male genetic fetus (XY chromosome) and the development of male secondary sex characteristics at puberty.
Clinical phenotypes vary from a normal male habitus with a mild spermatogenic defect or reduced secondary terminal hair; to a complete female habitus despite a Y chromosome.
Women (XX chromosomes) heterozygous for the androgen receptor gene have typical primary and secondary sexual characteristics.
This female carrier will pass the affected androgen receptor gene to any child with a 50% chance.
The androgen insensitivity syndrome is the largest individual entity that leads to 46 XY and inframasculinized genitalia.
The androgen receptor, which is defective due to a mutation in most of these syndromes, is a type of nuclear receptor that is activated by binding to androgenic hormones (testosterone or dihydrotestosterone) in the cytoplasm.
And then translocates to the nucleus where it joins the DNA, provided that elements of androgenic response and coactivators are present.
This combination functions as a transcription complex to activate androgen gene expression.
Therefore, the androgen receptor activates these genes to mediate the effects of androgens in the human body, including the development and maintenance of the male sexual phenotype and generalized anabolic effects.
More than 400 androgen receptor mutations have been reported.
The androgen insensitivity syndrome is divided into three categories differentiated by the degree of genital masculinization: the syndrome of complete androgenic insensitivity is indicated when the external genitalia are those of an average woman.
The mild androgen insensitivity syndrome is indicated when the external genitalia is those of an average male.
And the syndrome of partial androgen insensitivity is indicated when the external genitalia is partially but not masculinized.
The management of the androgen insensitivity syndrome is currently limited to symptomatic treatment.
Currently, there is no method available to correct the malfunctioning androgen receptor proteins produced by mutations of the androgen receptor gene.
Management areas include sex assignment, genitoplasty, gonadectomy about tumor risk, hormone replacement therapy, genetic counseling, and psychological counseling.
Yolk androgen levels in certain birds have been positively correlated with the social domain later in life.
Androgens bind and activate androgen receptors to mediate most of their biological effects.
It is determined by considering all biological test methods (around 1970).
The 5α-dihydrotestosterone was 2.4 times more potent than testosterone to maintain the average weight of the prostate and lumen mass of the duct (this is a measure of the stimulation of epithelial cell function).
While 5α-dihydrotestosterone was as potent as testosterone in preventing prostate cell death after castration.
It has also been found that androgens signal through membrane androgen receptors, distinct from the classical nuclear androgen receptor.
Androgens are synthesized from cholesterol and are produced mainly in the gonads (testes and ovaries) and the adrenal glands. The testicles produce a much higher amount than the ovaries.
The conversion of testosterone to the most potent 5α-Dihydrotestosterone occurs in the prostate gland, liver, brain, and skin.
Androgens are metabolized mainly in the liver.
A low testosterone level ( hypogonadism ) in men can be treated with testosterone administration.
Prostate cancer can be treated by eliminating the primary source of testosterone: removing the testicles (orchiectomy); or using agents that prevent androgens from accessing their receptor: antiandrogens.
Anabolic steroids, also known as anabolic-androgenic steroids (AAS), are steroidal androgens that include natural androgens such as testosterone and synthetic androgens that are structurally related and have similar effects to testosterone.
The word anabolic, which refers to anabolism, comes from the Greek ἀναβολή anabole.
Androgens or anabolic-androgenic steroids are three types of sex hormone agonists; the others are estrogens such as estradiol and progestogens such as progesterone.
Anabolic-androgenic steroids were synthesized in the 1930s and are now used therapeutically in medicine to stimulate muscle growth and appetite, induce male puberty, and treat chronic wasting conditions, such as cancer and AIDS.
The American College of Sports Medicine recognizes that anabolic androgenic steroids, in a proper diet, can contribute to increased body weight, often as lean mass increases and gains in muscle strength are achieved through high-intensity exercise.
A proper diet can be further increased by using anabolic-androgenic steroids in some people.
Liver damage (mainly with most oral anabolic-androgenic steroids) and dangerous changes in the structure of the heart’s left ventricle.
Anabolic-androgenic steroids can also cause conditions related to hormonal imbalances such as gynecomastia and reduced testicular size.
In women and children, anabolic androgenic steroids can cause irreversible masculinization.
Its use is known as doping and is prohibited by most major sports bodies.
For many years, anabolic-androgenic steroids have been the most commonly detected doping substances in laboratories accredited by the International Olympic Committee.
In countries where anabolic androgenic steroids are controlled substances, there is often a black market where smuggled, clandestine, or even counterfeit products are sold to users.
Androgen replacement therapy
Androgen replacement therapy (ART), often called testosterone replacement therapy, is a hormone replacement therapy in which androgens, usually testosterone, are replaced.
It usually involves the administration of testosterone through injections, skin creams, patches, gels, or subcutaneous granules.
As men enter middle age, they may notice changes caused by a relative decrease in testosterone: fewer erections, fatigue, thinning of the skin, decreased muscle mass and strength, and more body fat.