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whether ovaries or testes develop from an indifferent gonad
- defined by the XX or XY
- is not necessarily identical with the phenotypic sex seen later in life
development of female or male structures
what someone considers to be their sex
Where do indifferent (non-determined) gonads develop from?
- the primitive gonadal streak on the genital ridge
- which is a condensation of tissue near the adrenal gland
From which part of the the indifferent gonad do ovaries develop? Testes?
- Ovaries develop from the Cortex
- Testes develop from the Medulla
- both do so at week 6 of embryonic/fetal development
- the non-differentiating portion of the primitive gonad regresses as the other develops
What kind of hormones do embryonic ovaries produce vs. embryonic testes?
- embryonic ovaries do NOT produce estrogens
- while embryonic testes produce testosterone
- & MIF to control further masculinization
What is the small amount of information that initiates the differences between a male & female?
the SRY Gene (Sex-determining Region of the Y chromosome) which when transcribed results in the Testis-determining factor (TDF) [also known as Sex-determining region Y (SRY) protein]
What does translocation of SRY to X chromosome results in?
- a male with XX karyotype
- b/c the majority of genetic information on the Y chromosome is common to females
Testis-determining factor (TDF)
- initiation of male sex determination in humans by initiating the transcription of several genes necessary for development of male characteristics in the embryo including testicular differentiation & formation of the internal male structures under the influence of Muellerian Inhibiting Substance (MIS)
- TDF → causes the medulla portion of the indifferent gonad to differentiate → testis → which secrete testosterone & MIS
In the newly developing testes, what hormone do Sertoli cells secrete?
Müllerian Inhibiting Factor (MIF) also known as Anti-Müllerian Hormone (AMH)
Müllerian Inhibiting Factor (MIF)
causes regression of the Müllerian duct (the female duct system, which if allowed would go on to form the uterus, fallopian tubes, & upper parts of vagina)
In the newly developing testes, what hormone do Leydig cells secrete?
promotes development of the vas deferens, epididymous, & other Wolffian duct derivatives (Wolffian = the male duct system)
- made by 5α-reductase in the testis & some local tissues from testosterone
- it induces the formation of the external genitalia & male secondary sex characteristics (penis, urethra, prostate)
- acts via the same receptor as testosterone, but has a much higher potency due to a ~50 fold increase in binding efficiency for the receptor
- it cannot be aromatized into estrogens (in contrast to testosterone)
What is DHT responsible for later in male life?
it potentiates the development of acne & male pattern baldness
- in genetic females the cortex of the indifferent gonad differentiates into the ovary
- the embryonic ovary secretes no estrogen
- b/c in female development no testosterone is synthesized/secreted, the Wolffian duct won't develop therefore by default the Müllerian duct develops into all those aforementioned female structures
- also the labia minora develops first - he mentioned that a few times incase it becomes important
When might one be able to visibly differentiate between male and female genitalia in the womb?
- 17 weeks for males
- ~20 weeks for females (internal)
- preterm females tend to have a more developed clitoris than other structures (eg. labia minora)
What is a significant cause of abnormally developed external somatic sex, aka having ambiguous (incompletely correct) male or female genitalia?
- errors in steroid synthesis
- (21-Hydroxylase, 17α-Hydroxylase, 18-Hydroxylase, 18-Oxidase, etc.)
- • Turner’s Syndrome – gonadal dysgenesis (XO)
- • Klinefelter’s Syndrome – seminiferous tubule dysgenesis (XXY)
Turner’s Syndrome (XO)
- affected individuals are externally phenotypically female but have rudimentary or absent gonads, short stature, & mild obesity w/ a characteristic nuchal fat pad of variable prominence
- these women undergo no sexual maturation at
- puberty, but this can be treated with hormonal supplementation
- they have normal intelligence but may have other congenital anomalies
Klinefelter’s Syndrome (XXY)
- affected individuals have male genitalia but abnormal seminiferous tubules such that they are sterile
- these men have an increased incidence of mental retardation
- seminiferous tubule dysgenesis (abnormal embryonic organ development)
Female Developmental Disorders
- • Iatrogenic (exposure to androgen, progestational agents during pregnancy)
- • Congenital virilizing adrenal hyperplasia of the fetus (21 hydroxylase deficiency)
Male Developmental Disorders
- • Androgen resistance
- • Defective testicular development
- • Congenital virilizing hyperplasia of the fetus
Congenital Virilizing Adrenal Hyperplasia
- caused by a defect in an enzyme involved the glucocorticoid or mineralocorticoid synthesis pathways, resulting in an overproduction of androgenic steroids & a lack of glucocorticoid &/or mineralocorticoids
- depending on the enzyme involved & the degree of lack of activity, this condition may present a life-threatening condition a few days after birth (males will present in shock - steroid crisis)
- when endocrine & gametogenic functions of gonads are able to allow reproduction
- there is initiation & continuation of changes in external sexual & internal reproductive structures for reproductive capacity
- has a variable onset (the average age of which has been decreasing for > 175 years)
What are the average ages of onset for male & female puberty in the U.S.?
- males: 9-10 y/o
- females 7 - 8 (African American) or 8 - 9
- (Caucasian) y/o
- a delayed puberty workup is called for at age 13 in females if there is a lack of menses onset & age 14 in males if there's absent testicular development
Stages in Male Puberty
- 1. pre-adolescence
- 2. testicular enlargement begins
- 3. penile enlargement
- 4. growth of the glans penis
- 5. completion into the appearance of adult
- also corresponds w/ the development of male pubic hair pattern (escutcheon) & laryngeal enlargement & increased rigidity (deeper voice)
What does the hypothalamic- pituitary-gonadal axis control in males?
- 1. spermatogenesis in seminiferous tubules of testes
- 2. androgen biosynthesis in Leydig cells of the testes
When do plasma testosterone levels in males max out?
- at around 26-27 years of age
Actions of Androgens
- bind to androgen receptors target tissues
- are required for normal sperm maturation, normal function of sex accessory glands (epididymis, seminal vesicles, prostate, & bulbourethral gland), the maintenance of male secondary sex characteristics, & are particularly important for regulating prostate size (benign prostatic hyperplasia (BPH))
What is the order of androgen potency (MOST → least)?
DHT → testosterone → androstenedione → DHEA
Stages in Female Puberty
- 1. Thelarche (breast development)
- 2. Pubarche (development of female pubic
- hair pattern)
- 3. Menarche (onset of menstruation)
How can menstrual periods initially be described?
- Variable in length
- Usually anovulatory
- Irregular in cycle
What's the difference between male stages of puberty & female?
the general stages of male puberty don't have to proceed in order whereas the female stages of puberty DO
In the beginning of female puberty, when & how is Gonadotropin Releasing Hormone (GnRH) released from the hypothalamus?
- it's released in a pulsatile manner the levels of which tend to peak at night & drop during the day for the start of puberty
Unlike in men, how do levels of gonadotropins in females change throughout a lifetime?
- as women age, GnRH, FSH, & LH increase (estrogen drops off after menopause though)
- the early development of secondary sexual
- characteristics without gametogenesis (aka (no spermatogenesis or ovarian development) caused by abnormal exposure of immature males to androgen or females to estrogen
True Precocious Puberty
- early but otherwise normal pubertal pattern of gonadotropin secretion from the pituitary
- can be constitutional, cerebral (posterior hypothalamic disorders), caused by tumors, infections, gonadotropin-independent precocity, or developmental abnormalities
Constitutional Precocious Puberty
- precocious puberty with no underlying
- is more common in females than in males
Fertilization in Humans
- normally occurs in ampulla of the Fallopian tube
- sperm has chemoattraction to the ovum & adheres to the Zona Pellucida
- the acrosomal reaction (breakdown of the acrosome) occurs, releasing proteases (eg. acrosin) that facilitate penetration
- fertilin mediates fusion to ovum membrane, & once fused, development starts & polyspermia is prevented
Changes in the Endometrium & Blastocyst in Preparing For Implantation
- before the embryo implants into the endometrium it receives nourishment from the uterine secretions: steroid dependent proteins, cholesterol, steroids, iron, & fat-soluble vitamins.
- glandular epithelium synthesizes matrix substances, adhesion molecules, & surface receptors for matrix proteins, all needed for implantation
- the blastocyst secretes Human Chorionic Gonadotropin (hCG) & other substances required for implantation
Human Chorionic Gonadotropin (hCG)
secreted by the blastocyst & acts as an immunosuppressive agent, has growth- promoting activity, as well as acts like an autocrine growth factor that promotes placental development
- forms when the blastocyst comes into contact with the uterine endometrium & surrounds the blastocyst
- it erodes the uterine endometrium, allowing the blastocyst to implant
- establishes the nutrient circulation between the embryo and the mother, establishing an interface between maternal blood & embryonic extracellular fluid, facilitating passive exchange of material between the mother and the embryo
What are the important functions of a placenta?
- 1. hormone production
- 2. gas transport & exchange (O2, CO2)
- 3. solute transport
- 4. storage of proteins, glycogen, iron, etc.
- 5. control of molecular passage (IgG is the only Ab that can cross the placenta)
What hormones are made by the placenta?
- human chorionic gonadotropin (hCG)
- human chorionic somatomammotropins (hCS1/ hCS2, or placental lactogens)
- peptide hormones + neuropeptides
- placental variants of all known hypothalamic
- releasing hormones
- refers to the fact that these 3 are metabolically & hormonally interconnected
- the placenta produces estrogen & progesterone for maintaining pregnancy health + pregnenalone for fetal steroid synthesis
- the mother supplies energy substrates for the fetus & cholesterol for placental pregnenalone synthesis
- the placenta metabolizes maternal steroids
- the fetus makes DHEAS (dehydroepiandrosterone sulfate) which is transferred back to the placenta for estrogen (estriol, estradiol) synthesis
- the fetus also synthesizes, cortisol, cortisone, & other needed hormones, & locally changes sulfated steroids to useful forms
Placental Hormone Synthesis
- b/c the mother cannot synthesize all hormones needed to support a pregnancy herself, the placenta is a significant supplier of progesterone & estrogens to help support the pregnancy
- HOWEVER the mother supplies the placenta w LDL cholesterol as the placenta alone can't make enough cholesterol to support steroid synthesis
- AND the placenta lacks hormones necessary for steroid synthesis - help comes from the fetus
Which hormones does the placenta lack and where in the fetus do they come from in the conversion of precursors to steroid hormones?
- planenta lacks 17α-hydroxylase & 17,20-desmolase for estrone & estradiol synthesis
- the placenta also lacks 16α-hydroxylase for estriol synthesis
- all the conversions can be made by the aforementioned enzymes found in the fetal adrenal gland & liver
Response of the Mother to Pregnancy
- ↑ blood volume & cardiac output
- ↑ alveolar ventilation
- ↑ weight gain
- ↑ demand for dietary protein, iron, & folic acid supplements are recommended
- recommended weight gain is in the range of 11.5-16 kg for most women (5 kg for intrauterine contents, 9 kg maternal contribution)