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MNE Exam 2 > Sex Steroid Synthesis > Flashcards

Sex Steroid Synthesis Flashcards

1
Q

Which hormones stimulate conversion of cholesterol to pregnenolone in the adrenal gland, ovary, and testis?

A

Adrenal: ACTH

Ovary & testis: Luteinizing Hormone (LH)

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2
Q

What are the 2 separate pathways of testosterone synthesis? (just the major step difference)
Which is preferred in humans?

A

1) Progesterone (d4) undergoes 3b-HSD & d5-4 isomerase from pregnenolone
2) d4-androstenedione (d5) undergoes 3b-HSD & d5-4 isomerase from DHEA
3) d4 pathway is preferred in humans

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3
Q

Which enzymatic components of sex hormone synthesis are included on the same enzymes?

A

1) 3b-HSD and d5-4 isomerase activity on same cytochrome P450 enzyme
2) 17a-hydroxylase & C17-20 lyase activity on same cytochrome P450 enzyme

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4
Q

What are the 3 major testosterone derivatives?

A

1) Dihydrotestosterone (DHT)
2) Androstanediol
3) Estradiol

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5
Q

How and where is DHT formed? Why is it important?

A

DHT is formed from testosterone via 5a-reductase in the target tissues (removed d5 double bond); requires NADPH. Important because DHT is the active androgen in many tissues, including prostate.

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6
Q

How is androstanediol produced?

A

Androstanediol is produced from DHT via 3a-reductase.

-The 3-ketone group is reduced to hydroxyl

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7
Q

How is estrogen produced?

A

Testosterone is converted to estrogen via aromatase, makes A-ring aromatic. Aromatic A-ring precludes existence of C19 (branched from C10) –> 18 carbons in estrogen

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8
Q

How is testosterone transported? How much is free?

A

Bind to TeBG (testosterone binding globulin), and weakly to albumin
1-3% free

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9
Q

Where is TeBG produces and what regulates its synthesis?

A

1) TeBG is made in the liver, glycosylated
2) Synthesis is stimulated by estrogens, liver disease, and hyperthyroidism
3) Synthesis is inhibited by androgens, advancing age, and hypothyroidism

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10
Q

How is DHT transported? How much is free?

A

TeBG, 1% free

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11
Q

How is estradiol transported?

A

Weak binding to TeBG

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12
Q

How are Estrone and Progesterone transported?

A

Estrone: Albumin
Progesterone: CBG (same affinity as cortisol)

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13
Q

How is testosterone synthesis hormonally regulated? 8 steps.

A

1) Hypothalamus produces GnRH
2) Pituitary releases LH and FSH
3) LH induces Leydig cells to produce testosterone via adenylate cyclase
a) Activates cleavage of cholesterol to pregnenolone
4) FSH induces Leydig cells to produce more LH receptors
5) Testosterone feeds back to inhibit GnRH and LH
6) FSH activates Sertoli cells to produce ABP, testosterone synergizes effect of FSH
7) ABP binds testosterone to help bathe seminiferous tubules: identical to TeBG w/ different glycosylation
8) Sertoli cells produce inhibin, a peptide hormone that inhibits FSH release from pituitary

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14
Q

What are the 5 processes that involve androgens?

A

1) Sexual differentiation
2) Spermatogenesis
3) Secondary sexual characteristics
4) Anabolic metabolism
5) Male pattern behavior

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15
Q

How do androgens interact with their receptors? What are 3 genes controlled by testosterone?

A

1) Androgen Receptor is Nuclear
2) Androgens diffuse into cell, sometimes converted to DHT which has higher AR affinity
3) AR then binds DNA and alters transcription
4) ABP, PSA, and a2u-globulin are controlled by testosterone

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16
Q

Describe primary hypogonadism

A

1) Testicular failure - no 2º sex characteristics/regression of them
2) Due to genetic deficiency of an enzyme required to produce testosterone

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17
Q

Describe secondary hypogonadism

A

Defective secretion of gonadotropins

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18
Q

Describe 5a-Reductase Deficiency

A

1) Inability to produce DHT
2) Internal male genitalia, female external
3) Inguinal testes cause masculinization at puberty due to LH surge
4) Urethra in female position
5) Blind vaginal pouch

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19
Q

Describe Complete Androgen Insensitivity Syndrome (CAIS) (testicular feminization syndrome)

A

1) No functional androgen receptors
2) XY genotype, produce testosterone
3) Complete feminization of external genitalia
4) No pubic or axillar hair
5) No neg feedback - excess testosterone converted to estrogen, leading to gynecomastia

20
Q

Describe benign prostatic hypertrophy

A

1) Occurs in 75% of med over age 60

2) Poorly understood, androgens & estrogens involved

21
Q

What 2 classes of steroids are produced by the ovary, and how many carbons do they have?

A

21-carbon progestins (progesterone)

18-carbon estrogens (estradiol, estriol, estrone)

22
Q

Describe the activity of aromatase.

A

1) Produces 17b-estradiol from testosterone
2) Performs 3 hydroxylations requiring O2 and NADPH
3) Includes mixed function P450 oxidase

23
Q

What are the precursor molecules for the 3 estrogens?

A

Estradiol: derived from testosterone

Estriol & estrone: derived from androstenedione

24
Q

What are the major hormones produced by the corpus luteum, theca cells, and granulosa cells?

A

Corpus luteum: progesterone & some 17b-estradiol
Granulosa cells: Major source of 17b-estradiol
Theca cells: 17a-hydroxyprogesterone, androstenedione, and testosterone

*Converted to estrone and 17b-estradiol in granulosa cells

25
Q

Besides the ovary, where else is aromatase active?

A

1) Brain
2) Skin
3) Fat

26
Q

What are the major sources of estrogen in males, pregnant females, and post-menopausal women?

A

Males: 80% from peripheral aromatization of testosterone
Preg Females: 50% from aromatization of adrenal androgens
Post-meno: Synthesis of estrone from adrenal androstenedione

27
Q

How are estrogens degraded?

A

Converted in liver to glucuronide or sulfate derivatives (not so efficiently)

28
Q

How are progestins degraded?

A

1) Liver converts progesterone to glucuronide form: pregnanediol-20-glucuronide
2) So efficient that oral progesterone has no effect in humans
3) Synthetic progestins are used that are metabolized more slowly

29
Q

Describe PCOS

A

1) Overproduction of androgens

2) Hirsutism, obesity, irregular menses, impaired fertility

30
Q

Describe leydig cell & arrhenoblastoma tumors

A

Produce testosterone

31
Q

Describe Granulosa-thecal cell tumors

A

Produce estrogens

32
Q

Describe intraovarian adrenal rests

A

Produce cortisol

33
Q

Describe hydatiform mole/choriocarcinoma

A

Produce huge amounts of hCG

34
Q

Describe Osteoporosis

A

Occurs after menopause, no more estradiol to protect bone mass. Estrone may be insufficient

35
Q

What is DES?

A

1) Estrogen receptor agonist marketed to prevent misscarriage (no real effect)
2) DES daughters have:
- Cervical/vaginal cancers
- Reproductive tract defects
- Pregnancy complications
- Infertility
3) DES sons have epididymal cysts

36
Q

How does tamoxifen work?

A

1) Tamoxifen is a selective ER antagonist
- leaves bone-saving property
- doesn’t stimulate growth
2) Binds to ER, causes conformational change so Helix 12 interacts with different coactivators

37
Q

Where are hormones produced in a pregnant female?

A

Placenta produces progesterone and estriol (ovary is inactive)

38
Q

Why are estrogens and progestins synthesized in separate tissues?

A
  • Progesterone is precursor to estradiol

- Need separate tissues so progesterone tissues are free of enzyme to convert it into estradiol

39
Q

Which hormone is responsible for baldness?

A

DHT

40
Q

Testosterone controls which 4 male processes?

A

1) Gonadotropin regulation
2) Spermatogenesis
3) Sexual differentiation
4) Wolffian stimulation

41
Q

DHT controls which 2 male processes?

A

1) External virilization

2) Sexual maturation at puberty

42
Q

Describe Partial Androgen insensitivity syndrome

A

Similar to complete insensitivity, but there is residual receptor activity, symptoms can be mild to severe

43
Q

What causes penis growth to stop?

A

Androgen receptor downregulation

44
Q

When can micropenis be treated?

A

Can be treated when androgen synthesis failed during puberty, so AR still exists in cells - treat with androgens

45
Q

How can erect penis length be measured?

A

1) Stretching (450g force)

2) Inject prostaglandin E1

46
Q

What causes gynecomastia in bodybuilders? Obese males? Pre-pubertal males?

A

1) Bodybuilders take exogenous testosterone, converted to estrogens
2) High aromatase activity in adipose tissue
3) Pre-pubertal males have high aromatase activity, leads to transient gynecomastia in 50%

MNE Exam 2 (9 decks)

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