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4) Metabolic Endocrinology > 12) Sex Differentiation > Flashcards

12) Sex Differentiation Flashcards

1
Q

What is the common primordium for external genitalia?

A

Urogenital sinus

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2
Q

What does the Mullerian duct become? Which sex possesses the Mullerian duct?

A
  • Females

- Oviduct, uterus, upper vagina

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3
Q

What does the urogenital sinus become in females?

A

Clitoris, vulva

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4
Q

What does the urogenital sinus become in males?

A

Penis, scrotum

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5
Q

What does the Wolffian duct become? Which sex possesses the Wolffian duct?

A
  • Males

- Epididymis, vas deferens, seminal vesicle

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6
Q

The removal of undifferentiated testes from male rabbit embryos produced what type of reproductive tract and genitalia?

A
  • Female reproductive tract

- Female genitalia

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7
Q

What type of reproductive tract and genitalia is produced from gonadectomised female embryos?

A

Female features

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8
Q

The testes are (necessary/not necessary) for male sexual differentiation.

A

necessary

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9
Q

The ovaries are (necessary/not necessary) for female sexual differentiation.

A

not necessary

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10
Q

The development of male features is hormone (dependent/independent).

A

dependent

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11
Q

The development of female features is hormone (dependent/independent).

A

independent

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12
Q

Is the development into a male or female the default pathway?

A

Female

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13
Q

What are the three pre-requisites for normal sex differentiation?

A

1) Normal intact chromosome complement
2) Fully functioning sex determination genes
3) Intact steroidogenic pathway and receptors

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14
Q

Why is sexual differentiation required in males?

A

Provision of sperm

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15
Q

Why is sexual differentiation required in females?

A
  • Provision of eggs
  • Internal fertilization
  • Pregnancy
  • Lactation
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16
Q

How are males and females different in terms of their chromosomes?

A
  • Males: XY

- Females: XX

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17
Q

True or False: the presence of the Y chromosome always produces a male phenotype.

A

True

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18
Q

What is Klinefelter syndrome? What are symptoms?

A
  • Two or more X chromosomes in males

- Sterility and small testicles

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19
Q

What is Turner syndrome? What are symptoms?

A
  • A female is partly or completely missing an X chromosome (XO)
  • Short stature, loss of ovarian function
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20
Q

Normally, chromosomes pair and cross-over at which sections?

A

They cross-over along ALL their length

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21
Q

How do X and Y chromosomes pair?

A

Y pairs with X only at one end (pairing region)

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22
Q

How do X and Y chromosomes cross-over?

A

There are RARELY crossing-over events between X and Y

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23
Q

What does the sry gene stand for?

A

Sex-determining region of the Y chromosome

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24
Q

Is the SRY gene retained in the pairing or non-pairing region?

A

In the non-pairing region of the Y chromosome

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25
Q

What occurs when the SRY gene is mis-paired, and transferred to the X chromosome?

A
  • Sperm produces an X chromosome with the SRY gene

- Fertilization by the sperm would produce an XX male

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26
Q

What occurs if the SRY gene is deleted or mutated in the Y chromosome?

A

Produces an XY female

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27
Q

23/24 of the mutations causing an XY female lie in which region?

A

DNA-binding domain (HMG box) of the SRY gene

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28
Q

An amino acid region of the SRY gene shows homology to a motif within the _______ proteins, which possesses DNA-binding activity.

A

high mobility group (HMG)

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29
Q

Is DAX1 contained on the X or Y chromosome? What is its function?

A
  • X chromosome

- Inhibits testicular development

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30
Q

What genes does the SRY gene inhibit?

A
  • WNT4

- DAX1

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31
Q

The expression of SRY leads to the expression of other genes, leading to ____.

A

AMH

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32
Q

What is AMH? What produces AMH?

A
  • Anti-mullerian hormone (Mullerian-inhibiting substance)

- Produced by Sertoli cells

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33
Q

The differentiation of the gonad by what genes results in Sertoli cells producing AMH, and Leydig cells producing testosterone?

A
  • SRY
  • SOX9
  • SOX3
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34
Q

How does testosterone affect the Wolffian duct?

A

Positive effect on the development of the Wolffian duct

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35
Q

Which component allows for the development of male external genitalia?

A

Dihydroxytestosterone (DHT) produced from testosterone

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36
Q

Which component allows for the development of female external genitalia?

A

The lack of DHT from the lack of testosterone

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37
Q

What is responsible for testicular descent?

A

Testicular hormones

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38
Q

What guides testicular descent?

A

Gubernaculum

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39
Q

What hormone allows for trans-abdominal descent of the testes?

A

AMH

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40
Q

What allows for inguino-scrotal descent of the testes to the scrotal position?

A

Testosterone

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41
Q

How does the gubernaculum guide testicular descent?

A
  • The gubernaculum swells, providing traction to the testes to pull them through the inguinal canal
  • The testes are pulled to the outside of the body
  • The gubernaculum shrinks and the inguinal canal seals
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42
Q

What are the effects of defects in testosterone synthesis or actions? (3)

A

1) Phenotypic female (XY)
2) No ovaries (testes, but infertile)
3) Blind-ending vagina

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43
Q

What is the cause of androgen-insensitivity syndrome? What are symptoms?

A
  • A lack of androgen receptors

- Lack of epididymis, vas deferences, presence of female external genitalia

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44
Q

What are possible causes for defects in testosterone synthesis or action?

A
  • StAR protein deficiency
  • Leydig cell hypoplasia
  • Deficiency in 17-hydroxylase, 17-lyase
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45
Q

Do individuals with androgen-insensitivity syndrome possess testes?

A
  • Yes, but they are contained within the abnominal cavity (cryptorchidism)
  • The gubernaculum cannot shrink, and the testes can’t be pulled through the inguinal canal
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46
Q

What is the treatment for androgen-insensitivity syndrome?

A
  • Surgery to correct the ambiguous genitalia

- Gonadectomy post-puberty

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47
Q

How does the quantity of aromatase differ in individuals with androgen-insensitivity syndrome?

A

High levels of aromatase

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48
Q

What is the effect of congenital adrenal hyperplasia?

A
  • Hyperplasia of the adrenal glands before birth, causing excessive androgen production
  • Masculinization of the external genitalia at birth
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49
Q

What is the most common defect in CAH?

A

21-hydroxylase deficiency

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50
Q

What are the effects of a deficiency in 21-hydroxylase? (3)

A

1) Low cortisol and aldosterone production
2) Reduced negative feedback onto the hypothalamic/pituitary axis
3) Increased androgen production

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51
Q

What allows for the sexual differentiation of the brain?

A
  • Testosterone is converted to estrogen by aromatase

- Estrogen binding to its receptor in the brain causes sexual differentiation

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52
Q

When does sexual differentiation of the brain occur? How does it vary among species?

A
  • Occurs during a “critical time period” during development

- The timing is variable by species

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53
Q

When does sexual differentiation of the brain occur in primates?

A

3 to 6 months pre-natally

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54
Q

What is the effect of gonadal steroids on the “indifferent” brain?

A

Masculinization

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55
Q

How may sexual differentiation of the brain affect structure and function?

A
  • Affects the propensity of psychiatric diseases

- Differences in brain activity patterns (apparent over wide range of cultures)

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56
Q

What is the effect of CAH on child play patterns? Why?

A
  • Tendency towards male play patterns

- Exposure to androgens in utero

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57
Q

Which center controls LH and FSH in males post-puberty?

A

Tonic center

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58
Q

Do males possess a surge center?

A

No, the surge center is defeminized and does not develop

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59
Q

Does testosterone freely enter the brain? Does estrogen?

A
  • Testosterone: yes (converted to estradiol)

- Estradiol: no

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60
Q

What occurs to estradiol produced by the fetal ovary?

A

Binds to alpha-fetoprotein

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61
Q

Which center controls LH and FSH in females post-puberty?

A

Surge center AND tonic center

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62
Q

What are the two functions of the gonads?

A

1) Gametogenesis

2) Hormonogenesis

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63
Q

What are the three functional outcomes of hormonogenesis?

A

1) Electrolyte homeostasis
2) Fuel and protein metabolism
3) Adiposity and muscle mass

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64
Q

The sex determination of the fetus requires the hypothalamic-pituitary-gonadal axis in which sex?

A
  • Required in males

- Not required in females

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65
Q

Sexual changes in puberty requires the hypothalamic-pituitary-gonadal axis in which sex?

A

Important in BOTH sexes

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66
Q

What is required for reproduction in females?

A

Sex hormones during pregnancy and parturition

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67
Q

Does menopause or andropause require the hypothalamic-pituitary-gonadal axis?

A

Important in BOTH sexes

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68
Q

How does testosterone vary during the fetal period? What is the function?

A
  • Rise in testosterone

- Associated with sexual differentiation

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69
Q

How does testosterone vary during the neonatal period? What is the function?

A
  • Rise in testosterone

- Function is unknown

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70
Q

How does testosterone vary during the pre-pubertal period?

A

Gonads are dormant in both sexes

71
Q

How does adrenal androgen expression vary in the life cycle?

A
  • On average, androgen expression increases until age 20, and decreases afterwards
  • Transient increase in androgens during puberty
72
Q

How do male plasma hormones vary through puberty?

A

Increase in FSH and LH, associated with an increase in testosterone

73
Q

How do female plasma hormones vary through puberty?

A

Increase in FSH and LH, associated with an increase in estradiol

74
Q

Define puberty.

A
  • The physiological, morphological, and behavioural changes that occur in the growing animal
  • Development of gonads/brain/phenotype as they change from adolescent to adult
75
Q

What characterizes the onset of puberty in females?

A

First menstrual cycle (menarche)

76
Q

What characterizes the onset of puberty in males?

A

First ejaculation (semarche)

77
Q

How are menarche and semarche associated with fertility in females and males?

A

Both of these events do NOT signify fertility

78
Q

What is the pulsatile pattern of GnRH release in adulthood? What is it during puberty?

A
  • Adult: 90 minutes

- Puberty: diurnal

79
Q

The ________ release of GnRH regulates sexual development.

80
Q

What evidence suggests that the pulsatile release of GnRH regulates sexual development?

A

1) FSH and LH are present in the pituitary, and GnRH in the hypothalamus, before the onset of puberty (but they are not released)
2) Gonads of children can be stimulated by pulsatile administration of GnRH

81
Q

Describe the release of GnRH prior to puberty.

A

GnRH neurons in both the tonic and surge centers of the hypothalamus release low amplitude and frequency pulses of GnRH

82
Q

Describe the release of GnRH after puberty in the female. What do the tonic and surge centers control?

A
  • Tonic center controls basal levels of GnRH

- Surge center controls the pre-ovulatory surge of GnRH

83
Q

Which sex possesses a surge center?

A

Only the female

84
Q

How does GnRH secretion vary at the onset of puberty?

A

Rise in GnRH (both in amplitude and frequency of the pulses)

85
Q

What causes the increase in pulses of GnRH secreted from the hypothalamus?

A

Decreased sensitivity of the TONIC CENTER to negative feedback from gonadal steroids

86
Q

How does the sensitivity of the tonic center vary during puberty?

A

Decreased sensitivity to negative feedback from gonadal steroids

87
Q

How does the sensitivity of the surge center vary during puberty?

A

There is no alteration in surge sensitivity

88
Q

If there is no alteration in the surge center’s sensitivity, how is surge release stimulated after puberty?

A

Before puberty, estrogen levels are not high enough to stimulate surge release

89
Q

What occurs as a result of an increase in GnRH during puberty?

A
  • Increase in pulses of LH and FSH

- Increase in steroid levels to support spermatogenesis and folliculogenesis

90
Q

What substance regulates the pulsatile secretion of GnRH from GnRH neurons?

A

Kisspeptin (KISS1)

91
Q

Kisspeptin is secreted from neurons whose cell bodies are located in which nuclei of the hypothalamus? (2)

A
  • Anteroventral periventricular (AVPV) nuclei

- Arcuate (ARC) nuclei

92
Q

Kisspeptin contributes to a positive feedback circuit alongside which substances?

A
  • Estradiol

- GnRH

93
Q

Describe the estradiol-kisspeptin-GnRH positive feedback circuit.

A
  • Rising levels of estradiol act to increase kisspeptin

- Kisspeptin amplifies GnRH neuron activity

94
Q

How do the levels of kisspeptin vary after the onset of puberty in females?

A
  • Fluctuate with the cyclical levels of estradiol

- To drive the generation of the pre-ovulatory GnRH/LH surge

95
Q

The (age/body weight) of puberty in girls has been changing, but the (age/body weight) has not.

A

age

body weight

96
Q

What is the critical body weight to allow for the activation of the hypothalamic-pituitary-gonadal axis?

A

47 kilograms

97
Q

How has the onset of puberty varied in the past century? Why?

A
  • The onset of puberty is becoming earlier

- Better nutrition and health allow girls to reach 47 kg faster

98
Q

What is the size of GnRH?

A

Decapeptide (10 amino acids)

99
Q

What is co-synthesized with GnRH in pre-pro GnRH?

A

GnRH-associated peptide (GAP)

100
Q

Which signal transduction mechanism allows for the stimulation of gonadotrophs by GnRH?

A
  • GPCR (PLC)

- Increase in calcium and PKC increases FSH/LH secretion

101
Q

How does a long-acting GnRH analog affect the pituitary secretion of LH?

A

Desensitization of the pituitary, due to the lack of pulsatility

102
Q

How does exogenous GnRH (when GnRH is absent) affect the pituitary secretion of LH?

A

Little or no gonadotrophin response

103
Q

GnRH is released alongside ___.

104
Q

Where do axons of GnRH terminate?

A

Hypophyseal portal capillaries

105
Q

What other tissues synthesize GnRH, apart from the hypothalamus? What is its function?

A
  • Placenta
  • Gonads
  • Breast
  • Lymphocytes
  • Pituitary
  • The function is unknown
106
Q

What is the common subunit of FSH and LH? The subunit is also shared with which hormones?

A
  • alpha subunit

- TSH and hCG

107
Q

What differentiates LH and FSH?

A

The B-subunit

108
Q

What creates different isoforms of LH and FSH with slightly different biological properties?

A
  • Changes in glycosylation that may occur in circulation

- LH and FSH are glycoproteins

109
Q

Which signal transduction mechanism does FSH utilize?

A
  • GPCR

- Adenylate cyclase

110
Q

Which signal transduction mechanisms does LH utilize?

A
  • GPCR

- Adenylate cyclase and PLC

111
Q

What are the target tissues of LH in the male and female?

A
  • Male: Leydig cells

- Female: Thecal cells

112
Q

What are the target tissues of FSH in the male and female?

A
  • Male: Sertoli cells

- Female: Granulosa cells

113
Q

The actions of LH and FSH are the same as which hormone? What is its target organ?

A

ACTH on the adrenal cortex

114
Q

What are the events of LH and FSH that are the same as ACTH on adrenal cortex cells?

A

1) Increase in intracellular cholesterol
2) Transport of cholesterol by StAR
3) Conversion to pregnenolone

115
Q

Which hormone(s) is/are steroidogenic in the testes? Which cells does it act upon?

A
  • LH

- Leydig cells

116
Q

Which hormone(s) is/are steroidogenic in the ovaries? Which cells does it act upon?

A
  • LH and FSH

- Several cell types (thecal cells and granulosa cells)

117
Q

What are the three important cell types in spermatogenesis?

A
  • Spermatogonia
  • Sertoli cells
  • Leydig cells
118
Q

Where are Sertoli cells located with respect to the seminiferous tubules? Where are Leydig cells located?

A
  • Sertoli cells are inside the seminiferous tubules

- Leydig cells are outside the seminiferous tubules

119
Q

What is the significance of the location of Sertoli cells?

A
  • Located inside the seminiferous tubules
  • Isolated from the immune system
  • Responsible for maintaining the environment of spermatogonia to produce sperm cells
120
Q

What are the most important androgens secreted by the testes?

A
  • DHEA

- Testosterone

121
Q

The contribution from the adrenal gland to the synthesis of androgens is less than _%.

122
Q

What are androgens synthesized from the testes bound to in circulation? Why must they be bound?

A
  • Albumin
  • Sex-hormone-binding globulin (SHBG)
  • Lipophiles must be bound in circulation
123
Q

Cells that do not contain active testosterone must convert testosterone to what?

A

Dihydroxytestosterone (DHT)

124
Q

Which type of testosterone may be converted to estradiol by target tissues? Which type cannot?

A
  • Testosterone can be converted

- DHT cannot be converted

125
Q

Which cells synthesize testosterone?

A

Leydig cells

126
Q

What is the intermediate compound between DHEA and testosterone?

A

Androstenedione

127
Q

What enzyme converts testosterone to estradiol?

128
Q

What enzyme converts testosterone to DHT?

A

5a-reductase

129
Q

When do occasional pulses of LH and FSH occur in young children?

A

Mainly nocturnal pulses

130
Q

If children produce occasional pulses of LH and FSH, why aren’t they able to produce secondary sex characteristics at puberty?

A

The production of steroid hormones is not high enough

131
Q

What occurs to spermatogonia during puberty?

A
  • Mitotic proliferation

- They begin to divide, and continue to do so throughout the adult life

132
Q

Describe the developmental steps to the production of spermatids.

A

1) Spermatogonia differentiates into a primary spermatocyte
2) Primary spermatocyte undergoes meiosis I to become a secondary spermatocyte
3) Secondary spermatocyte undergoes meiosis II to become a spermatid

133
Q

What is the function of Sertoli cells in spermatogenesis?

A
  • Secretion of steroidal mitotic factor and androgen binding protein
  • Concentration of testosterone in the seminiferous tubules
134
Q

Where does sperm further mature?

A

In the seminiferous tubules and epididymis

135
Q

What is the most frequent cancer in men in industrialized countries?

A

Prostate cancer

136
Q

What metabolite is elevated in prostate cancer?

137
Q

What is the function of the prostate in terms of sperm development?

A
  • Prostate excretes a serine protease (prostate specific antigen)
  • PSA inactivates the sperm motility inhibitor
138
Q

What occurs to the prostate in later life in dogs and humans?

A
  • Prostate encircles the urethra and enlarges during later life
  • Eventually, restricts urine flow
139
Q

What is the surgical treatment for issues with the prostate in old age?

A

Enlarge the urethra and remove part of the prostate

140
Q

What is the medical treatment for issues with the prostate in old age?

A
  • Treat with anti-androgens

- Suppression of testosterone suppresses the enlargement of the prostate

141
Q

Why is the treatment of anti-androgens effective in older men with an enlarged prostate?

A
  • Prostate is more responsive to testosterone in old age

- Due to an increased number of receptors

142
Q

What allows for the detection of prostate cancer?

A

Rectal palpation and/or PSA

143
Q

Which hormones act directly to control testicular function? Which hormone acts indirectly?

A
  • FSH and testosterone act directly

- LH acts indirectly by stimulating the Leydig cells to produce testosterone

144
Q

What is the function of androgen binding protein?

A
  • Bioconcentrates testosterone in the seminiferous tubules and epididymis
  • Promotes spermatogenesis and maturation
145
Q

___ facilitates the last stages of spermatid maturation.

146
Q

____ and _________ are required for the maturation of spermatids to spermatozoa.

A

LH and testosterone

147
Q

__ is not required for the gametogenesis in the male. _____________ may be used instead.

A

LH

exogenous testosterone

148
Q

What are current methods for male contraceptives?

A
  • Vasectomy

- Condoms

149
Q

What are characteristics of an ideal male contraceptive?

A
  • Rapidly effective and fully reversible
  • Does not interfere with other testosterone-dependent processes
  • Has no short or long-term side effects
  • Has no impact on eventual offspring
  • Be acceptable for both partners
150
Q

Where does spermatogenesis occur?

A

Seminiferous tubules in the testes

151
Q

What is the overall mechanism of spermatogenesis?

A

Diploid spermatogonia undergo a series of divisions and differentiation to form haploid spermatozoa

152
Q

Where are haploid spermatozoa mainly stored?

A

Epididymis

153
Q

How long is the spermatogenesis process?

A

60 to 70 days

154
Q

Which androgen is involved in spermatogenesis? Where is it produced and what does it act on?

A
  • Testosterone from Leydig cells

- Acts on Sertoli cells

155
Q

What is the function of FSH in spermatogenesis?

A
  • Acts on Sertoli cells to increase ABP in testes

- Allows a high concentration of testosterone in the seminiferous tubule

156
Q

What are most male hormonal contraceptions based on?

A

The usage of exogenous androgen and progestogen to suppress LH and FSH by increasing negative feedback

157
Q

What occurs with the depletion of LH and FSH in males?

A
  • Depletion of intra-testicular testosterone and ABP
  • Decreased testosterone in the seminiferous tubules
  • Spermatogenesis is inhibited
158
Q

What must male contraceptives provide to maintain libido and secondary sex characteristics?

A

Peripheral testosterone

159
Q

What occurs after stopping male hormonal contraception?

A

Gradual recovery of spermatogenesis over months

160
Q

What are side effects of male hormonal contraception?

A
  • Acne

- Higher levels of testosterone

161
Q

Male hormonal contraception have similar side effects to what?

A

Drug abuse of anabolic steroids by athletes

162
Q

What are other male hormonal treatments that may be used?

A
  • GnRH antagonists and testosterone
  • FSH antagonists
  • Inhibin agonists
163
Q

How often is GnRH released?

A

Pulses occur every 90 minutes

164
Q

What is the regulator of negative feedback of GnRH, LH, and FSH?

A
  • GnRH: testosterone
  • LH: testosterone
  • FSH: inhibin
165
Q

What is inhibin produced by?

A

Sertoli cells in response to FSH

166
Q

What is the function of inhibin?

A

Selective reduction of the amount of FSH produced

167
Q

How does the function of activins differ from inhibins?

A
  • Activins stimulate FSH release

- Inhibins inhibit FSH release

168
Q

What chains produce inhibins? What chains produce activins?

A
  • Inhibin: alpha + beta
  • Activin: beta + beta
  • Alpha and beta chains are encoded by different genes
169
Q

Which sex utilizes both inhibin A and inhibin B? Which sex utilizes only inhibin B?

A
  • Women: inhibin A and inhibin B

- Men: inhibin B

170
Q

Are estrogen and progesterone responsible for a stimulatory or inhibitory effect in the female?

A

They are responsible for both, depending on the stage of the cycle

171
Q

A defect in spermatogenesis is the cause in about __% of cases of lack of conception.

172
Q

What are causes of male infertility?

A
  • Lack of LH or FSH secretion
  • Overproduction of prolactin
  • Primary failure of testes (cryptorchordisn)
  • Reduced sperm motility
  • Autoimmune response to sperm
  • Chromosomal abnormality
173
Q

What is the result of an overproduction of prolactin in males?

A

Testicular involution

174
Q

Which chromosomal abnormality may result in male infertility? What is the karyotype?

A
  • Klinefelter syndrome

- 47XXY

4) Metabolic Endocrinology (15 decks)

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