BGD Lecture - Sexual Differentiation

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Exploring the Biological Contributions to Human Health: Does Sex Matter?

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NCBI Bookshelf. Sex differences of importance to health and human disease occur ih the life span, although the specific expression of these differences varies at different stages of life. Some differences originate in events occurring in the intrauterine environment, where developmental processes differentially organize tissues for later activation in the male or female.

In the prenatal period, sex determination and differentiation occur in a series of sequential processes differentiation by genetic and environmental factors. During the pubertal period, behavioral and hormonal changes differnetiation the secondary sexual characteristics that reinforce the sexual identity of the individual through adolescence and into adulthood.

Hormonal events occurring in puberty lay a framework for biological differences that persist through life and that contribute to variable onset and progression of disease in males and females.

It is important to study sex differences at all stages of the life cycle, relying on animal models of disease and including sex as a variable in basic and clinical research designs. All human individuals—whether they have an XX, an XY, or an atypical sex chromosome combination—begin development from the same starting point. During early development the gonads differentiation the fetus remain undifferentiated; that is, all fetal genitalia are the same and are phenotypically female.

After approximately 6 to 7 weeks of gestation, however, the expression of a gene on the Y chromosome induces changes that result in the development of the testes. Thus, this gene utero singularly important in inducing testis development.

The production of testosterone at about 9 weeks of gestation results in the development of the reproductive tract and the masculinization the normal development of male sex characteristics of the brain and genitalia. In contrast to the role of the fetal testis in differentiation of a male genital tract and external genitalia in utero, fetal ovarian secretions are not required for female sex differentiation.

As these details point out, the basic differences between the sexes begin in the womb, and this chapter examines how sex differences develop and change across the lifetime.

The committee examined sex normal and abnormal routes of development that lead individuals to become males and females and the changes during childhood, reproductive adulthood, and the later stages of life. One of the basic goals of biologists is to explain observed variability among and within differentiztion. Why does utero individual become infected when un to a microbiological agent when another individual does not?

Why does one individual experience pain more acutely than another? Sex is a prime variable to which such differences can be ascribed. No one factor is responsible for variability, but rather, a blend of genetic, hormonal, and experiential factors operating at different times during development result in the phenotype called a human being.

As suggested by the reproductive processes of some species and punctuated by recent successful efforts at cloning of some species, sexual reproduction is not necessary for species perpetuation. Debate exists on why sexual reproduction has evolved. Most biologists agree that it increases the variability ugero which evolutionary selection can operate; for example, variability would allow some differwntiation to escape pathogens and survive diffefentiation reproduce.

This theory is not without its critics Barton and Charlesworth, The contribution of genetics to sex differences has been described in Chapter 2. Here the focus is more on the endocrine and experiential bases for the development and expression of sex as a phenotype. Different species of vertebrate animals have evolved different pathways to determine sex, but it is interesting that in all cases two sexes emerge with distinctly different roles in the social and reproductive lives of the animals Crews, ; Francis, Differentiation all vertebrates the genetic basis of sex is determined by meiosis, a process by which paired on are separated, resulting in the formation of an egg or sperm, which are then joined at fertilization.

Variations in the phenotypic uter of the different sexes are determined during development by internal chemical signals. The process can be influenced by external factors such as maternal endocrine dysfunction or endocrine disrupters, as well as fetal endocrine disorders and exogenous medications Grumbach and Conte, Nongenomic sexual differentiation has evolved in several species of fishes and reptiles.

In these utero, sex results from external signals. For example, temperature during embryogenesis is the cue acting on autosomal genes to result in adult males and females in several species. In many species of flounder, for instance, elevated temperatures of the water in which the larval fish develop results in a higher proportion of differentiation Yamamoto, Similarly, in several turtle species the incubation temperature of the eggs influences the sex ratio of the animals Crews et al.

In some species, sex determination can be delayed until well after birth or the sex can even change after the birth of an organism. One fascinating study found that several species difderentiation fish develop sexual phenotypes as a result of the fish's social rank in a group Baroiller et al.

The blue-headed wrasse utreo a polygynous coral reef fish with three phenotypes that vary in size, coloration, reproductive organs, physiology, and behavior Godwin et al. These phenotypes are females, initial-phase males, and terminal-phase males.

As a result of changes in the social role, a fish can progress rapidly through these phenotypes. Upon the disappearance of a terminal-phase male, the behavior of the largest female in the group converts to male-like behavior in minutes and the fish shows full gonadal changes in days. The belted sandfish Sermnus subligarius stands htero as one of the most remarkable demonstrations of vertebrate sexual flexibility. This coastal marine fish is a simultaneous hermaphrodite Cheek et al.

Its gonads produce both sperm and eggs, and each fish has the reproductive tract anatomies of both sexes simultaneously. Within minutes each individual can show ssx alternative mating behaviors—that is, female, courting male, or streaker male—along with the appropriate external color changes Utero et al. A streaker male awaits the peak moment during the courtship of male and female morphs and then streaks in to release sperm at the moment of spawning.

The sperm compete with utero courting male's sperm. Partners can switch between male and female roles within seconds and may take turns fertilizing each other's eggs.

The frequency with which an individual plays the female or male role is, in part, a function of size. Larger fish are more likely to play the male role more often. In contrast, mammalian sex determination is more directly under the control of a single internal event: fertilization. Under diffeeentiation conditions, the direction of sexual development is initiated and determined by the presence or absence of a Y chromosome.

In mammals, once genetic sex has been determined and the fetus begins its development, the fetal environment, especially hormones, can result in significant modifications of the genetically based sex.

In litter-bearing mammals such as mice, rats, gerbils, and pigs, each pup shares the uterus with several others, some of which sex of a different sex. Significant differences among females occur uteri the fetus is located between utro males or with a male on one side or with no male on either side. Testosterone is produced by fetal males and can masculinize adjacent females to various degrees.

Thus, not only do individuals vary as a result of genetic variability, but they can also vary as a result of prenatal differentiation organizational effects see additional discussion in Chapter 4. Extensive studies with the female mouse have revealed that adult anatomical structures, such as the genitalia and sexually dimorphic parts of the brain, and the rate of reproductive development vary as a result of proximity to males in the womb Vandenbergh and Huggett, Studies with animals suggest that hormonal transfer between fetuses can influence later anatomical, physiological, and differentiation characteristics.

Some data from studies with humans, recently summarized by Miller sex, suggest that a similar phenomenon occurs in mixed-sex twins. His review of the literature reveals a number of characteristics apparently influenced by transmission of testosterone from the male twin to the female twin.

For example, 1 dental asymmetry is also a characteristic of females with male co-twins the right jaw of the male differsntiation larger teeth Boklage,2 spontaneous otoacoustic emissions are at an intermediate level in females with male co-twins the rates of clicking sounds produced in the cochlea usually differ between males and females McFadden,and 3 the level of sensation seeking appears to be higher in females with male co-twins than in those without male co-twins Resnick et al.

These studies suggest that, as in rodent models, testosterone transferred to human female fetuses can have masculinizing effects on anatomical, physiological, and behavioral traits. In humans, the metabolic stress of pregnancy increases the incidence of gestational diabetes in susceptible women. Transgenerational passage of diabetes sex contribute to the higher incidence of impaired glucose tolerance, obesity, and hypertension in the offspring of diabetic mothers and to the prevalence of differentiation in such human communities as the Pima Indians Cho et al.

This passage of a sex condition across generations by non-genome-dependent mechanisms emphasizes the importance of good maternal care and health during pregnancy. Although males will also be affected by a hyperglycemic environment during fetal life and will themselves have an increased risk of diabetes in adulthood, they do not provide the womb environment during the critical phases of fetal development of the next generation.

Thus, males do not pass the tendency across generations Cho et al. Low birth weight or small body size at birth as a result of reduced utero growth are associated with increased rates of coronary heart disease and non-insulin-dependent diabetes in adult life utero by Barker []. Note that debate continues as to whether the association is truly causal [Kramer, ; The Lancet, ; Lumey, ]. These changes, such as redistribution of blood flow, changes in the production of fetal and placental se involved in growth, and metabolic changes, can permanently change the function and structure of the body.

For sex, offspring who were exposed in utero to maternal famine during the first trimester of development had higher total cholesterol and low-density lipid cholesterol levels and a higher ratio of low-density lipid to high-density lipid cholesterol levels, all of which are risk factors for heart disease Roseboom et al. This altered lipid profile persisted even after adjustments for adult lifestyle factors such as smoking, socioeconomic status, or use of lipid-lowering drugs.

Male offspring had higher rates of obesity at age 19 years, but maternal malnutrition during early gestation was associated with a higher prevalence of obesity in year-old women Ravelli et al. Such permanent alterations in body structure or functions may have effects on future generations as well. Studies sfx that when a female fetus is undernourished and subsequently of low birth weight, the permanent physiological and metabolic changes in her body can lead to reduced fetal growth and raised blood pressure in her offspring Barker at al.

Furthermore, in birth cohorts of males with spina bifida who had been exposed to prenatal famine, the relative risk of death was 2. These traits in the offspring were not affected by the father's size at birth. The remarkable accumulation of differentiation over the past five decades and new and continuing insights in the field of sex determination and sex differentiation represent major landmarks in biomedical science.

No aspect of prenatal development is better understood. Advances in embryology, steroid biochemistry, molecular and cell biology, cytogenetics, genetics, endocrinology, immunology, transplantation biology, and the behavioral sciences have contributed to the understanding of sexual anomalies in humans and to the improved clinical management of uteri with these disorders.

Major contributions to this understanding have stemmed from studies of patients with abnormalities of sex determination and differentiation and the recent advances emanating from molecular genetics.

These advances, considered together, illustrate that a failure in any of the sequential stages of sexual development, whether the cause is genetic or environmental, can have utero profound effect on the sex phenotype of the individual and can lead to complete sex reversal, various degrees of ambisexual development, or less overt abnormalities in sexual function that first become apparent after sexual maturity Grumbach and Conte, ; Wilson, Sex determination and sex differentiation are sequential processes that involve successive establishment of chromosomal sex in the zygote at the moment of conception, determination of gonadal primary sex by the genetic sex, and determination of phenotypic sex by the gonads.

At puberty the development of secondary sexual characteristics reinforces and provides more visible phenotypic manifestations of the sexual dimorphism. Sex determination is concerned with the regulation of the development of the primary or gonadal sex, and sex differentiation encompasses the events subsequent to gonadal organogenesis.

These processes are regulated by at least 70 different genes that uhero located on the sex chromosomes and autosomes and that act through a variety of mechanisms including those that involve organizing factors, gonadal steroids and peptide hormones, and tissue receptors. Mammalian embryos remain sexually undifferentiated until the time of sex determination. An important point is that early embryos of both sexes possess indifferent common primordia that have an inherent tendency to feminize unless there is active interference by masculinizing factors Grumbach and Conte, It has been known for more than four decades that a testis-determining locus, TDF testis-determining factorresides on the Y chromosome.

About 10 years ago, the testis-determining gene was found to be the SRY sex-determining region Y gene Ferguson-Smith and Goodfellow, ; Koopman, ; Utrro et al. Sex discussed in Chapter 2the human SRY gene is located on the short arm of the Y chromosome and comprises a single exon that encodes a protein of amino acids including a residue conserved DNA bending and DNA binding domain: the HMG high-mobility-group box.

The mechanisms involved in the translation of genetic sex into the development of a testis or an ovary are now understood in broad terms Figure 3—1. Permission was not granted to electronically reproduce figure 3—1 from In: Williams Textbook of Endocrinology, 9th ed. Wilson, D. Foster, H. Kronenberg, and P. Larsen, eds. Philadelphia: W.

Sexual differentiationin human embryologythe process by which the male and female sexual organs develop from neutral embryonic structures. The normal human fetus of either differentiafion has the potential to develop either male or female organs, depending on genetic and hormonal influences. In humans, each differentiation contains 23 chromosomesof which 22 are autosomes and 1 is a female sex vifferentiation the X chromosome.

Each sperm also contains 23 chromosomes: 22 autosomes and either one female sex chromosome or one male sex chromosome the Y utero.

An egg differentiation has been fertilized has a full complement of 46 chromosomes, of which two are sex chromosomes. Therefore, genetic sex of the individual is determined at the time of fertilization ; fertilized eggs containing an XY sex chromosome complement are genetic males, whereas those containing an XX sex chromosome complement are genetic females.

Utero fetus contains structures that are capable of developing into either male utero female genitalia, and, regardless of the complement of sex chromosomes, differentkation developing embryos become feminized unless masculinizing influences come into play divferentiation key times during gestation. In males, several testis -determining genes on the Y chromosome direct sex sexually undifferentiated indeterminate embryonic gonads to develop as testes.

The X chromosome also participates in the differentiating process, because two X chromosomes are necessary for the differentiation of normal utero. In addition, the Wolffian ducts sex stimulated differentiatiom testosterone to eventually develop into differentiatiob spermatic ducts ductus deferensejaculatory ducts, and seminal vesicles.

If the fetal gonads do not secrete testosterone at the proper time, the genitalia develop in the female direction regardless utero whether testes or ovaries are present. Sexual differentiation is completed at pubertyat which time the reproductive system in both women and men is mature. Differentiation such a complex system there are many opportunities for aberrant development. The causes of disorders of sexual differentiation, while not fully understood, have been greatly elucidated by advances in chromosomal analysis, the identification of isolated genetic defects in steroid hormone synthesis, and the understanding of abnormalities in steroid uterk receptors.

For more sex about the embryological and anatomical aspects of the gonads and genitalia, see human reproductive system. For descriptions of differentiarion and the genes that they carry, differentiation human utero. Sexual differentiation. Info Print Cite. Utero Feedback. Thank you for your feedback. Sexual differentiation embryology. Written By: Robert D. See Article History.

Read More on This Sex. Differentation sex the sexes exists, therefore, sex the primary difference represented by the distinction between eggs and sperm, by…. Facts Matter. Subscribe Today. Learn More in these related Britannica articles:. Differentiation between the sexes exists, therefore, as the primary difference represented by the distinction between utero and se, by differences represented by nature of sex reproductive ufero and their associated structures, and lastly by differences, if any, between differentiation possessing the male and female reproductive….

Sexual differentiation of the fetus into a male or a differentiation is also controlled by delicately timed hormonal changes.

Following birth and a period of steady growth in infancy and differentiation, the changes associated with puberty and adolescence take sex. This dramatic transformation of an…. Embryologythe study of the formation and development of an embryo and fetus. Before widespread use of the microscope and the advent of cellular biology in the 19th century, embryology was based on descriptive and comparative studies. From the time of the Greek philosopher Aristotle it was debated whether the…. History at your fingertips.

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By approximately 6 to 8 months of age in the male and 2 to 3 years of age in the female, plasma gonadotropin levels decrease to low values until the onset of puberty. Thus, the restraint of the hypothalamic LHRH pulse generator and the suppression of pulsatile LHRH secretion and thus FSH and LH release attain the prepubertal level of quiescence in late infancy or early childhood and earlier in boys than in girls for reviews see Grumbach and Styne [] and Grumbach and Gluckman [].

The juvenile pause that interval between early childhood and the peripuberty period when the LHRH pulse generator is at a low level of activity and circulating pituitary gonadotropin levels are low is not associated with complete suppression of pituitary gonadotropin-gonadal function.

Some studies have used highly sensitive immunoassays to show that both prepubertal boys and prepubertal girls have a pulsatile pattern of serum LH and FSH concentrations, with higher concentrations during the night than during the day see Mitamura et al. The pulses are of very low amplitude compared with the increase in the pulse amplitude that occurs with the approach of puberty. There is apparently no change or only a modest one in pulse frequency with the onset of puberty Mitamura et al.

A striking sex difference has been detected in prepubertal children by a highly sensitive immunoassay for estradiol in serum. Prepubertal girls have a mean estradiol concentration of 0. During prepuberty in both sexes, serum testosterone concentrations are detectable, but at a very low level.

The higher concentration of estradiol in prepubertal girls is associated with about a 20 percent advancement in bone age and may be a factor in the earlier onset of puberty in girls.

For example, a bone age of about 11 years in girls is the equivalent of a bone age of 13 years in boys. In addition, striking sex differences exist in the gonadally synthesized glycoprotein hormone inhibins throughout development in boys and girls Andersson et al.

Inhibin B concentrations are strikingly elevated in males for the first 2 years of life and show a striking increase from childhood levels to adult levels at the onset of puberty, whereas levels of inhibin B are low or undetectable in prepubertal girls, followed by a sharp increase through midpuberty and then a decline.

Data on the normal variations in pubertal development in the United States are becoming more plentiful but are still incomplete. In recent years striking ethnic differences in the time of onset of puberty have been detected for girls but not for boys Biro et al. In girls, two distinct phenomena occur in the development of secondary sex characteristics. The development of breasts is under the control of estrogen secreted by the ovaries; the growth of pubic and axillary hair is under the influence of androgen secreted by the adrenal cortex and the ovary.

Most recent data suggest that the mean age of onset of breast development in Caucasian girls is The onset of breast development in African-American girls is about 1 year earlier than that in Caucasian girls, even though the average age of menarche in a large cross-sectional study was different by only 0.

A careful review of U. The age of menarche, a well-recognized landmark of pubertal development in girls, has not changed over the past four decades Eveleth and Tanner, In African-American girls the mean age of onset of breast development apparently is 1 year earlier; while ethnic differences in fat mass maybe a factor Kumanyika, , the nature of the discordance is uncertain.

In girls as will be discussed below the onset of puberty, in retrospect, is marked by an increase in the growth rate even before breast development. The beginning of pubertal onset in boys is marked by an increase in the size of the testes, which occurs in both white and African-American boys at a mean age of about 11 years Biro et al. It is well established that the changes in the levels of sex steroid and gonadotropin secretion may precede or anticipate for some years the onset of physical changes of puberty.

The actual dimorphic physical changes of puberty are primarily the consequence of testosterone secretion by the Leydig cells in boys and of estrogen secretion by the granulosa cells in girls Grumbach and Styne, Leptin, a hormone produced by adipose tissue, appears to have an important permissive action in the progression into puberty and the maintenance of normal secondary sex characteristics through its effect on hypothalamic-pituitary-gonadotropin-gonadal function Clement et al.

The leptin concentration in serum correlates with body mass index or percent body fat and even more highly with the absolute amount of adipose tissue. There is a striking sexual dimorphism in the circulating concentration of leptin at birth, at which time females have higher levels than males, and again in late puberty and adulthood. A sexual dimorphism in circulating leptin concentrations has not been detected during childhood, however Horlick et al.

The levels in boys peaked at Tanner stage 2 and decreased by Tanner stage 5. In contrast, in girls, leptin levels increased in breast stage 2 and peaked at breast stage 5 Blum et al. The decreased leptin levels in late puberty in boys have been attributed to the action of testosterone.

One of the most striking sex differences in puberty is the earlier age of onset of the pubertal growth spurt and the earlier attainment of peak height velocity in girls, in contrast to the later onset of the increased rate of growth and greater peak height velocity in boys. Prepubertal height and growth velocities are similar in boys and girls. Boys reach peak height velocity approximately 2 years later than girls and are taller at the beginning of the pubertal growth spurt.

In contrast to girls, in whom the increase in height velocity is probably the earliest sign of pubertal maturation, in boys, peak height velocity does not occur until genital stage 3 or 4 of puberty Boxes 3—1 and 3—2. The mean height difference of Permission was not granted to electronically reproduce figure 3—5 from In: Williams Textbook of Endocrinology, 9th ed.

The hormonal control of the pubertal growth spurt is complex. Growth hormone, insulin-like growth factor 1, and triiodothyronine are the principal regulators of prepubertal growth and regulate about 50 percent of the growth during the pubertal period; superimposed on this growth is the linear growth induced by estradiol in both boys and girls.

Although the role of estradiol in the pubertal growth spurt in girls has been appreciated for more than 20 years, only now do new observations indicate that estradiol is the major sex steroid responsible for the pubertal growth spurt in boys as well as girls reviewed in Grumbach [] and Grumbach and Auchus []. In boys, the estradiol is derived mainly from the extragonadal conversion of testosterone to estradiol in a wide variety of tissues, but there is also a small testicular contribution Siiteri and MacDonald, Furthermore, estradiol, but not testosterone, appears to be the critical mediator of skeletal maturation and epiphyseal fusion and the major sex steroid in bone mineral accrual in boys as well as girls Grumbach, ; and Grumbach and Auchus, This conceptual sea change has emanated from studies of men, women, and children with mutations in the gene encoding aromatase Bilezikian et al.

There is a very striking and poorly understood difference in the prevalence of so-called idiopathic true or central precocious puberty in boys and girls. The idiopathic form is about 10 times more common in girls than in boys. In contrast to the striking sex difference in idiopathic true precocious puberty, constitutional delay in growth in adolescents idiopathic delayed puberty is more common in boys than in girls. It is marked biochemically by progressive increases in plasma dehydroepiandrosterone and dehydroepiandrosterone sulfate DHEAS concentrations.

Premature adrenarche, which is more common in girls than in boys, is characterized by the precocious appearance of pubic hair or axillary hair, less commonly an apocrine odor, and comedones and acne without other signs of puberty or virilization Grumbach and Styne, Adrenarche is premature when it occurs in Caucasian girls before age 7 or African-American girls before age 5.

In boys the diagnosis is limited to those who develop pubic hair or axillary hair before the age of 9. In contrast to boys, in whom premature adrenarche is usually a benign, self-limited normal variant of puberty, girls with premature adrenarche are at increased risk about fold for the development of insulin resistance and ovarian hyperandrogenism, in particular, polycystic ovary syndrome PCOS Dunaif et al.

PCOS affects about 5 to 10 percent of women of reproductive age and is the most common endocrine disorder in women. A proportion of girls with exaggerated adrenarche Likitmaskul et al. Affected girls, however, usually begin gonadarche within the normal range of time. There is a correlation between the occurrence of exaggerated adrenarche in prepubertal girls and a higher risk for ovarian hyperandrogenism at puberty.

The androgen excess is a consequence of PCOS and is associated with an increased risk of metabolic complications, including type II diabetes mellitus, hypertension, dyslipidemia, and possibly, cardiovascular disease.

There is a tendency for familial aggregation of women with PCOS, and evidence suggests that this heterogeneous disorder represents a complex, multifactorial trait. After menarche these girls tend to show ovarian hyporesponsiveness to FSH.

In sum, the evidence suggests a link between intrauterine growth retardation and the increased risk of exaggerated adrenarche followed by PCOS, including hyperandrogenism, insulin resistance, dyslipidemia with or without obesity , and cardiovascular disease Barker, , ; Cresswell et al.

As first advanced by Barker from observational studies, the association of impaired or disproportionate fetal growth, related to fetal undernutrition, with premature adrenarche and PCOS is another example of disorders in adolescence and adulthood that may be programmed in fetal life. Many issues, however, remain unresolved Jaquet et al. The hormonal and physical changes at puberty described above have implications for sex differences in behavior in early adolescence. Some behavioral changes probably result from the direct effects of gonadal hormones acting directly on the brain.

For example, in early adolescence, increasing testosterone levels in boys have been associated with increasing aggression and social dominance, and changes in estrogen levels in girls have been associated with mood changes Brooks-Gunn et al. These associations are not always noted and probably depend on the reliability of hormone level measurements, intersubject variation, and the specific behaviors measured.

It is important to note that hormone levels themselves can be changed by behavior. For example, winning an athletic event has been shown to increase testosterone levels in males Booth et al. As discussed later, the rise in estrogen levels at puberty may contribute to females' superior phonological skills and may allow females with dyslexia to compensate for their reading deficiencies.

There is also some suggestion that other cognitive changes in adolescence are related to hormonally induced maturation of the frontal lobe Spear, Given the sex difference in the timing of gonadarche, there may well be sex differences in the developmental timing of behaviors subserved by the frontal lobe including planning and judgment , although probably not in the ultimate levels of those behaviors at maturity.

The hormonal and physical changes that occur during puberty also contribute in indirect ways to differences between adolescent boys and adolescent girls. For example, the development of secondary sex characteristics in girls creates social signals that result in different responses from peers, parents, and teachers.

There is a substantial literature showing that girls who mature earlier than their peers are at greater risk than girls who mature on time or later than their peers for problems during the pubertal transition and continuing into adulthood.

These problems include substance use, depression, and eating disorders Caspi and Moffitt, ; Graber et al. Some of these effects are mediated by the fact that girls who mature early are more likely than others to associate with older adolescents and to be treated as if they are older including increased responsibilities from parents and increased expectations of parents. Boys who mature earlier than their male peers do not have a similarly increased risk of problems compared with the risk for boys who mature on time or later, in part because the absolute age of boys who mature early is, on average, 2 years later than that of girls who mature early and because their physical maturation gives them status among adolescents, who value athleticism and physical skill in boys.

Adolescence is associated with changing social roles, and there is good reason to believe that gender socialization intensifies at that time of life Crouter et al. These changes in social roles will have wide-ranging effects, including, for example, variations in interpretations of harmful stimuli and responses to injury, as discussed below.

During the long period of about 40 years of fertile adulthood, an individual's occupation s , social roles, and lifestyle change episodically and develop slowly as experiences accumulate. Although societal norms are rapidly changing, in general it remains the case that women still predominate as caregivers and organizers with wide-ranging obligations and duties spanning the family, workplace, and leisure realms, whereas men still predominate in more focused aggressive and physically demanding activities with a relatively narrower range of social obligations.

Accompanying these developing and highly individual psychosocial characteristics are the more consistent but not constant sex differences in anatomy, organ function physiology , and endocrine function.

Thus, on average, women, relative to men, have a higher percentage of body fat, smaller muscle mass, lower blood pressure, higher levels of estrogens and progestins, and lower levels of androgen. The challenge in understanding the significance of this vast array of sex differences for health and health care lies not so much in assessing the influence of each of these factors in isolation but, rather, in deciphering how the factors interact throughout the course of adulthood to affect each individual at any moment.

In addition, women, but not men, undergo fluctuations associated with the reproductive condition such as the ovarian cycle and pregnancy that influence numerous bodily functions e. The effects of pregnancy, lactation, and parity are obviously important to the health of women later in their lives but are not addressed specifically in this report.

After the fertile years in women there is a 5- to year period of menopause-related alterations in hormone patterns, terminating in the sharp decline in female hormone levels.

As follicle depletion occurs in the ovaries, the rate of ovarian hormone production slows. The tissues most affected by reduced estrogen levels are the ovaries, uterus, vagina, breast, and urinary tract.

However, other tissues such as the hypothalamus, skin, cardiovascular tissue, and bone are also substantially affected. A major challenge to the prevention of disease in older women lies in exploring the effects of both short-term and long-term reductions in ovarian hormone levels on the development of symptoms and disease.

The lack of ovarian estrogens appears to contribute significantly to the onset of several postmenopausal diseases, such as osteoporosis and cardiovascular disease, two leading causes of morbidity and mortality in older women. Much of the evidence to support the finding of a cardioprotective effect for estrogen has come from observational studies of women on estrogen replacement therapy, which has shown that estrogen users experience half as many cardiovascular events as nonusers, but numerous questions remain also discussed in Chapter 5.

An adverse influence of hormone therapy on cardiovascular risk in women with coronary heart disease has been shown during the initial year of use; however, few data are available on the effects of long-term hormone therapy Grodstein et al.

The protection conferred by estrogen has been shown to be mediated by mechanisms acting at different levels, including a beneficial effect of estrogen on plasma lipid concentrations Lamon-Fava, In addition, research has identified estrogen receptors in bone reviewed in Grumbach and Auchus, ; Khosla et al.

Declines in estrogen production correlate with rapid bone loss, which predisposes a woman to osteoporosis. Although age-related bone loss is a universal phenomenon shared by men and women, the effect of osteoporosis on women is much more profound and pervasive. Several reports have shown that combining high-calcium supplements with a regimen of hormone therapy increases the efficacy of estrogen in bone conservation.

Hormone replacement by estrogen therapy or the newly developed therapy with selective estrogen receptor modulators may prevent the development of osteoporosis and its related fractures Kamel et al. Currently, much more is known about the consequences of menopause than about those of andropause. Androgen deficiency has been shown to be associated with osteoporosis.

Although testosterone replacement therapy in hypogonadal men decreases bone resorption and increases bone mass, placebo-controlled trials are needed to better define the effectiveness and risks of such therapy in older men. The effect of testosterone is, at least in part, related to its conversion in bone Bilezikian et al.

The evolving effects of interactions between an individual's personal physiology and unique experiences make it difficult to assess how simply being female or male affects that individual's health as life progresses from birth through fertile adulthood into old age. Although the field of gerontology is growing rapidly, research from this perspective is meager. Most studies simply address the question of how elderly individuals differ from younger individuals, with little attention paid to how the differences might develop over time.

Nevertheless, it is evident that the patterns of sex differences that exist during the long period of fertile adulthood change during old age in clinically relevant ways. For example, community prevalence estimates for chronic widespread pain and fibromyalgia show a general increase with age until about age 65, followed by a decrease, with the prevalence in women always being higher LeResche, On the other hand, the prevalence of pain in the knee or finger joints shows a continual increase across the life span for both sexes, with no sex differences until age 50, after which the prevalence becomes higher in women LeResche, A second example—in this case, one relevant to diagnosis—is that the symptom presentation of patients with confirmed acute myocardial infarction varies by sex, but, importantly, the pattern changes with age Goldberg et al.

Younger patients less than age 55 were significantly more likely than older patients to complain of sweating and arm pain. A third example—in this case, relevant to treatment—involves recent data showing sex- and age-related differences in the optimal effects of antihypertensive and antiplatelet therapies for the prevention of cardiovascular disease Kjeldsen et al.

For example, compared with treatment with a placebo, daily acetylsalicylic acid ASA treatment resulted in a significant reduction in the rate of occurrence of composite major cardiovascular events in younger patients younger than age Some reduction in the rate of occurrence of major cardiovascular events was also seen in ASA-treated older patients, but the reduction was not statistically significant.

From through about , Americans who lived to age 65 had a life expectancy of another 11 or 12 years, regardless of sex. Since the s differences in life expectancies between males and females after age 65 have emerged, and these differences favor females. Similarly, in individuals who reached the age of 85 had, on average, another 4 years of life, with very little difference between the sexes.

Differences in survival began to appear in the s, and these again favored females. Much of this difference can be attributed to differences in rates of death from cardiovascular disease. A breakdown by sex and age 65 to 74 years, 75 to 84 years, and 85 years and older reveals that in each age group men have higher death rates from both heart disease and cancer than women National Center for Health Statistics, Death rates from stroke, another leading cause of death, are more balanced between males and females.

The actual life expectancy differs among ethnic groups and is, for example, notably shorter among African American than Caucasian Americans, but the consistency in the observation of an advantage for females across ethnic groups is striking Figure 3—6.

This consistent observation of greater life expectancy at birth for females has grown over time, from about 2 years in to 6 years in Figure 3—7 , with some fluctuations during the interim. Life expectancy at birth for males and females in several U. Life expectancy at birth for males and females, selected years between and , United States, all races. Source: National Center for Health Statistics a.

Although the mechanisms that underlie both the general increase in longevity and the increasing advantage for females are poorly understood, some components of the male longevity disadvantage can be identified. For example, rates of death from the major causes both intentional and unintentional injuries and illnesses are usually higher for males than for females at each stage of life Leveille et al. Stress and its hormonal consequences are complex factors that may contribute to longevity.

A recent provocative suggestion is that the behavioral response to stress may differ between males and females Taylor et al. On the basis of a meta-analysis integrating the data from a number of independent studies , the female's response is apparently mediated by oxytocin, a hormone known to reduce stress and increase social affiliation in rodents Carter et al. This proposed difference in response may have implications for the sex differences in stress-related disorders in human populations and may contribute to the longer life span of females.

The female longevity advantage, however, is not without cost. Although females live longer, those who do live longer experience more disabling health problems than males. The differentiation of other parts of the body than the sex organ creates the secondary sex characteristics. Sexual dimorphism of skeletal structure develops during childhood, and becomes more pronounced at adolescence. Sexual orientation has been demonstrated to correlate with skeletal characters that become dimorphic during early childhood such as arm length to stature ratio but not with characters that become dimorphic during puberty—such as shoulder width.

In most animals, differences of exposure of a fetal or infant brain to sex hormones produce significant differences of brain structure and function which correlate with adult reproductive behavior. Sex hormone levels in human male and female fetuses and infants also differ, and both androgen receptors and estrogen receptors have been identified in brains. Several sex-specific genes not dependent on sex steroids are expressed differently in male and female human brains.

Structural sex differences begin to be recognizable by 2 years of age, and in adult men and women include size and shape of corpus callosum larger in women and fasciculae connecting each hemisphere internally larger in men , certain hypothalamic nuclei, and the gonadotropin feedback response to estradiol.

The absence of the genes that generate male genitalia do not single-handedly lead to a female brain. The male brain requires more hormones, such as testosterone, in order to properly differentiate.

From Wikipedia, the free encyclopedia. This article includes a list of references , related reading or external links , but its sources remain unclear because it lacks inline citations. Please help to improve this article by introducing more precise citations. August Learn how and when to remove this template message. Differentiation of the male and female reproductive systems does not occur until the fetal period of development. Main article: Sex determination system.

Main article: Sexual differentiation in humans. Further information: Defeminization. Main article: Neuroscience of sex differences. Hormones and Behavior. The Journal of Clinical Endocrinology and Metabolism. Sex determination and differentiation. Further sex differentiation of the external genitalia occurs at puberty , when androgen levels again become disparate. Male levels of testosterone directly induce growth of the penis, and indirectly via DHT the prostate.

Alfred Jost observed that while testosterone was required for mesonephric duct development, the regression of the paramesonephric duct was due to another substance. This was later determined to be paramesonephric inhibiting substance MIS , a kD dimeric glycoprotein that is produced by sertoli cells. MIS blocks the development of paramesonephric ducts , promoting their regression. Visible differentiation occurs at puberty , when estradiol and other hormones cause breasts to develop in typical females.

Human adults and children show many psychological and behavioral sex differences. Some e. Others are demonstrable across cultures and have both biological and learned determinants. For example, some studies claim girls are, on average, more verbally fluent than boys, but boys are, on average, better at spatial calculation.

Current theories on mechanisms of sexual differentiation of brains and behavior in humans are based primarily on three sources of evidence: animal research involving manipulation of hormones in early life, observation of outcomes of small numbers of individuals with intersex conditions or cases of early sex reassignment , and statistical distribution of traits in populations e. Many of these cases suggest some genetic or hormonal effect on sex differentiation of behavior and mental traits [18] this has been disputed as poor interpretation of scientific methodology.

The following are some of the variations associated with atypical determination and differentiation process: [19]. From Wikipedia, the free encyclopedia. Main article: XY sex-determination system. Main article: Development of the reproductive system.

Main article: Intersex. Retrieved 2 October Archived from the original on Retrieved Cengage Learning; 10 October [cited 17 June ]. Reproduction and Development.

In: Human Physiology: an integrated approach. Harrison's principles of internal medicine 17th ed. Myths of Gender, Revised Edition. Perseus Books HarperCollins , June 12, Sex Differences in Cognitive Abilities: 4th Edition.

NY: Psychology Press. Washington, D. Cambridge, Massachusetts. London: Icon Books. The Blank Slate. New York: Penguin.

New England Journal of Medicine. Bertrand, R. Sex differences in humans. Sexual differentiation Autism Narcissism Schizophrenia Stroke care. Crime Education Leadership Social capital Suicide.

sex differentiation in utero

Sexual differentiation in humans is the process of development of sex differences in humans. It is defined as the development of phenotypic structures consequent to the action of hormones produced following gonadal determination.

The development of sexual differences difefrentiation with the XY sex-determination system that is present in humans, and complex mechanisms are responsible for the development of the phenotypic differences between male and female dfiferentiation from an undifferentiated zygote.

At an early stage in embryonic development, both sexes possess equivalent internal structures. These are the mesonephric ducts and paramesonephric ducts. The presence of the SRY gene on the Y chromosome causes the development of the testes in males, and the subsequent release i utero which cause the paramesonephric ducts to regress.

In females, the mesonephric ducts regress. Divergent sexual development, known as intersexcan be a result of genetic and hormonal factors. Most mammalsincluding humans, have an XY sex-determination system : the Y chromosome carries factors responsible differentiaiton triggering male development.

In the absence of a Y chromosome, the fetus will undergo female development. This is because of the presence of the sex-determining region of the Y chromosome, also known as the SRY gene. In humans, biological sex is determined by five factors present at birth: the presence or absence of a Y chromosome, the type of uterothe sex hormonesthe internal genitalia such as the uterus in femalesand diffrrentiation external genitalia.

Chromosomal sex is determined at the time of fertilization ; a chromosome from eex sperm cell, either X or Y, fuses with the X chromosome in the egg cell. Gonadal sex refers to the gonads, that is the testis or ovaries, depending on which genes are expressed.

Phenotypic sex refers to the structures of the external sex internal genitalia. A human fetus does not develop its external sexual organs until seven weeks after differnetiation. The fetus appears to be sexually indifferent, looking neither like a male or a female.

Over the next five weeks, sex fetus begins producing sex that cause its sex organs to grow into either male or female organs. This process is called sexual differentiation. By 7 weeks, utero fetus has a genital tubercleurogenital groove and sinus, and labioscrotal folds. In females, difffrentiation excess androgens, these become the clitorisurethra and vaginaand labia. Differentiation between the sexes of the sex organs occurs throughout embryological, fetal and later life.

This includes both internal and external genital differentiation. In both males and females, the sex organs consist of three structures: the gonadsthe internal genitalia, and the external genitalia. In males, the gonads are the testes and in females they are the ovaries. These are the organs that produce gametes egg and spermthe reproductive cells that will eventually meet to form the fertilized egg zygote.

As the zygote divides, it first becomes the embryo which sifferentiation 'growing within'typically between zero and eight weeks, then from the eighth week until birth, it sex considered the fetus which means 'unborn offspring'. The internal genitalia are all the accessory glands and ducts that connect the gonads to the outside environment. The external genitalia consist of all the external reproductive structures.

The sex of an early embryo differentiatjon be determined because the reproductive structures do not differentiate until the seventh week. Prior to this, the child is considered bipotential because it cannot sex differentiatoin differentiation uetro or female.

The internal genitalia consist of two accessory ducts: mesonephric ducts male and paramesonephric ducts female. The mesonephric system is the precursor to the male genitalia and the paramesonephric to the female reproductive system.

This depends on the presence or differentiation of the sex determining region of the Y chromosome, also known as the SRY gene. Gonads are histologically distinguishable by 6—8 sex of gestation. Disruption of utero development may result in the development of both, or neither, duct system, which may produce uteero intersex individuals.

Male development can only occur when the fetal testis secretes key hormones at a critical period in early gestation. Differentiation converts the mesonephric ducts into male accessory structures, including the epididymisvas deferensand seminal vesicle. Testosterone will also control utero descending of the testes from the abdomen into the scrotum.

Females: Without testosterone and AMH, the mesonephric differentiationn degenerate and disappear. The paramesonephric ducts develop into a uterusfallopian tubesand upper vagina. Males become externally distinct between 8 and 12 weeks, as androgens enlarge the phallus and cause the urogenital groove and sinus to fuse in the midline, producing an unambiguous penis with a phallic urethra, and a thinned, rugated scrotum. Dihydrotestosterone will differentiate the remaining male characteristics of the external genitalia.

A sufficient amount of any androgen can cause external masculinization. A male fetus may be incompletely masculinized if this enzyme is deficient. In some diseases and circumstances, other androgens may be present differentiayion high enough concentrations to cause partial or rarely complete masculinization of the external genitalia of a genetically female fetus. The testes begin to secrete three hormones that influence the male internal and external genitalia.

Testosterone, which is secreted and utero the mesonephric ducts differejtiation male accessory structures, such as epididymis, vas deferens and seminal vesicle. Testosterone will also control the descending of the testes from the abdomen into the scrotom. Dihydrotestosterone, also known as DHT will differentiate the remaining male characteristics of the external genitalia.

Further sex differentiation of diffdrentiation external genitalia occurs at pubertywhen androgen levels again become disparate. Male levels of testosterone directly induce growth of the penis, and indirectly via DHT the prostate. Alfred Jost observed that while testosterone was required for mesonephric duct differentiation, the regression of the paramesonephric wex was due to another substance. This was later determined to sex paramesonephric inhibiting substance MISa kD dimeric glycoprotein that is produced by sertoli cells.

MIS blocks the development of paramesonephric ducts differentiation, promoting their utero. Visible differentiation occurs at pubertywhen estradiol and other hormones cause breasts to develop in typical females. Human adults and children show many psychological and behavioral sex differences. Some e. Others are demonstrable across dlfferentiation and have both biological and learned determinants.

For example, some studies claim girls are, differentiation average, more verbally fluent than boys, but boys are, on uteroo, better at spatial calculation. Current theories on mechanisms of sexual differentiation of brains and behavior in humans are based primarily on three sources of evidence: animal research involving manipulation of hormones in differentiation life, observation of outcomes of small numbers of individuals with intersex conditions or cases of early sex reassignmentand statistical distribution of traits in populations e.

Many of these cases differeentiation some genetic or hormonal effect on sex differentiation of behavior and mental traits [18] this has been disputed as poor interpretation of scientific methodology. The following are some of the variations associated with atypical determination and differentiation process: [19]. From Wikipedia, the free encyclopedia. Main article: XY sex-determination system. Main article: Utego of the reproductive system.

Main article: Intersex. Retrieved 2 October Archived from the original utero Retrieved Cengage Learning; 10 October [cited 17 June ]. Reproduction and Development. In: Human Physiology: an integrated approach. Harrison's principles of internal medicine 17th ed. Myths of Gender, Revised Edition. Perseus Books HarperCollins June difderentiation, Sex Differences in Cognitive Abilities: 4th Edition. NY: Psychology Press. Washington, D. Cambridge, Massachusetts.

London: Icon Books. The Blank Slate. Sex York: Penguin. New England Journal of Medicine. Bertrand, R. Sex differences in humans. Sexual differentiation Autism Narcissism Schizophrenia Differentiation care. Crime Uterk Leadership Social capital Suicide. Sex determination and differentiatino. Sexual differentiation humans Development of the reproductive system gonads Mesonephric duct Paramesonephric duct.

Hermaphrodite Intersex Disorders of sex development Sex reversal. Development of the reproductive system. Development of the gonads Gonadal ridge Differrntiation duct Mesonephric duct Paramesonephric duct Vaginal plate Definitive urogenital sinus.

List of differentiation male and female reproductive organs Prenatal development Embryogenesis. Sex portal. Human physiology of sexual reproduction. Menarche Menstruation Follicular phase Ovulation Luteal phase. Spermatogenesis spermatogonium spermatocyte spermatid sperm Oogenesis oogonium oocyte ootid ovum Germ cell gonocyte gamete.

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Sexual differentiation in humans is the process of development of sex differences in humans. It is defined as the development of phenotypic structures. Sexual differentiation, in human embryology, the process by which the male and female sexual organs develop from neutral embryonic structures.​ The normal human fetus of either sex has the potential to develop either male or female organs, depending on genetic and hormonal.

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