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Hormone Biosynthesis Flashcards

1
Q

Rate limiting step in steroidogenesis

A

Transfer of cholesterol from outer mitochondrial membrane to inner

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2
Q

Responsible for cholesterol transport across mitochondrial membrane

A

STAR

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3
Q

Congenital lipoid adrenal hyperplasia (mutation, location, inheritance, functional change)

A

Loss of function mutation in STAR, chromosome 8, AR, limited intracellular transport of cholesterol 000? intracellular lipid accumulation 00> cellular destruction

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4
Q

Locations of steroid synthesis

A

Mitochondrial membrane, cytoplasm, endoplasmic reticulum

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5
Q

Locations of steroid receptor

A

Nucleus, cytoplasm

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6
Q

Mechanism of steroid hormone transport across cell membrane

A

Simple diffusion

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7
Q

Characteristics of steroid hormones

A

Small, non-polar, lipophilic

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8
Q

G-protein receptors

A

cAMP, calcium messenger, protein kinase/MAP kinase

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9
Q

cAMP second messenger hormones

A

FSH, LH, HCG, ACTH, TSH, CRH

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10
Q

Calcium second messenger hormones

A

GnRH, TRH, LH, kisspeptin

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11
Q

Protein kinase/MAP kinase hormone

A

Oxytocin

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12
Q

cAMP receptor function

A

o Hormone binds cell membrane receptor
o Adenylate cyclase activated
o Gα-GTP subunit binds catalytic unit forming active enzyme converting ATP to cAMP
o Forms cAMP-receptor protein complex which activates protein kinase A (PKA)
o Inactive form: tetramer, 2 regulatory subunits and 2 catalytic subunits
o Bound: Catalytic units released, regulatory units form dimer
o Catalytic units phosphorylate serine and threonine residues of cellular proteins (enzymes and mitochondrial, microsomal, and chromatin proteins) (energy-producing)
o Physiologic effect
o Enzyme activity terminated by hydrolysis of GTP to GDP returning the enzyme to its inactive state

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13
Q

Calcium messenger receptor function

A

o Phospholipase C (PLC) catalyzes hydrolysis of polyphosphatidylinositols (IPI2) into two intracellular messengers: IP3 (inositol triphosphate) and DAG (diacylglycerol)
o IP3 binds with a receptor in the smooth ER and mitochondria and opens the Ca2+ channel
o DAG activates protein kinase C
o Calmodulin binding Ca2+ causes a conformational change
o Modifies calcium transport, enzyme activity, calcium regulation of cyclic nucleotide and glycogen metabolism and secretion and cell motility

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14
Q

Single transmembrane domain receptor types

A

Tyrosine kinase, cytokine, serine/threonine kinase

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15
Q

Tyrosine kinase receptor hormones

A

Insulin, IGF, EGF, PDGF, FGF

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16
Q

Cytokine receptor hormones

A

GH, PRL, hPL, leptin

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17
Q

Serine/threonine kinase

A

Activin, inhibin

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18
Q

Tyrosine kinase receptor function

A

o 3 domains: extracellular domain for ligand binding, single transmembrane domain, cytoplasmic domain
o Receptor has 2 alpha and 2 beta subunits (each w/ 3 domains as above) linked by disulfide bridge
o Ligand specificity determined by unique AA sequence that determines 3D conformation
o Ligand binding –> conformational change of cytoplasmic domain –> autophosphorylation

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19
Q

Cytokine receptor second messenger

A

JAK-STAT

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20
Q

Serine/threonine kinase receptor second messenger

A

SMAD4 –> FOXH1

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21
Q

A/B Regulatory Domain

A

 Amino acid terminal
 Most variable in superfamily (i.e. only 18% homology between ERα and ERβ)
 In ER-α contains TAF1 which can stimulate transcription in absence of hormone binding

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22
Q

C DNA Binding Domain

A

 Most homologous
 Hormone binding induces conformational change in the 3 helices allowing binding to HRE (hormone responsive elements) of target genes
 Contains 2 zinc fingers: determine specificity for binding to enhancer site in gene promoter

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23
Q

D HInge REgion

A

Contains nuclear localization signal

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24
Q

E Hormone Binding Domain

A

Harbors TAF2 which requires hormone binding for full activity
Functions:
o Pocket for hormone binding
o Sites for cofactor binding
o Responsible for dimerization
o Harbors TAF-2
o Binding site for HSP (when no hormone bound)

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25
Q

F Carboxy Terminal

A

no notes

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26
Q

TAF1 location/function

A

(A/B, regulatory domain) can stimulate transcription in the absence of hormone when fused to DNA

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27
Q

TAF2 location/function

A

(E, hormone binding domain) must have hormone binding for full activity

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28
Q

TAF3 location/function

A

(B-upstream segment [BUS]) autonomously activates transcription OR synergizes w/ other TAFs

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29
Q

TAFs on ER’s

A

ERα has TAF1 and TAF2

ERβ only has TAF2

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30
Q

TAFs on PR’s

A

PRα has TAF1 and TAF2

PRβ has TAF1, TAF2, and TAF3

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31
Q

Steroid hormones with nuclear receptors

A

Estrogen, progesterone, androgens, thyroid (alpha-chrom 17, beta-chrom3), retinol, vit D

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32
Q

Steroid hormones with cytoplasmic receptors

A

MIneralocorticoids, glucocorticoids

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33
Q

Steroid hormones with receptors in cytoplasm which move to nucleus after hormone binding

A

Corticosteroid

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34
Q

ER receptor expression during menstrual cycle

A

Peak late proliferative (self induced by E2), declines in early secretory (increased P4), increased in mid- and late-secretory (decreased P4)

35
Q

ER alpha dominant tissues

A

Uterus, breast, bone, hypothalamus, pituitary, adrenal (E2 and EE most sensitive)

36
Q

ER beta dominant tissues

A

Granulosa cells, brain, CV system, colon

37
Q

ER alpha and beta tissues

A

ovary, breast (alpha in dev and fxn, beta as natural suppressor of alpha activity)

38
Q

2 SERMS and MOA

A

Raloxifene, tamoxifen; competitive inhibitor of estrogen binding to ER

39
Q

Tamoxifen SEs

A

VTE, vaginal bleeding, endometrial hyperplasia/cancer, hot flashes, cataracts

40
Q

Raloxifene SEs

A

Hot flashes, vaginal dryness, VTE (less than tamoxifen), decreases LDL, increase HDL, no change in TG

41
Q

Raloxifene location of estrogenic and antiestrogenic effect

A

Estrogenic effect on bone

Antiestrogenic effects on breast and uterus

42
Q

Tamoxifen location of estrogenic and antiestrogenic effect

A

Estrogenic: liver (decrease AT3, total chol, LDL, increase binding globulins, stimulates P4-R synthesis), bone, vaginal mucosa, endometrium
Antiestrogenic: cystostatic at breast, cytotoxic with breast ca

43
Q

PR-alpha action and TAFs

A 
Negative action (inhibits activity of PR-B)
TAF1 on reg domain, TAF2 on hormone binding domain
44
Q

PR-beta action and TAFs

A

Positive reg of progesterone response genes

TAF1 on reg domain, TAF2 on hormone binding domain, TAF3 in B-upstream segment (BUS) at 5’ terminal

45
Q

PR receptor expression

A

Induced by E2, inhibited by P4

Peak late-proliferative phase, nearly undetectable by midpoint of secretory phase

46
Q

First gen progestins

A

Estranes derived form testosterone

Pregnanes derived from 17-OHP

47
Q

Second gen progestins

A

Gonanes derived from testosterone

48
Q

Third gen progestins

A

Gonane (levonorgestrel) derivatives

49
Q

Fourth gen progestins

A

Non-ethylated estranes

50
Q

Estranes

A 
Norethindrone (MIcronor)
Niorethindrone acetate (Loestrin)
Ethynodiol diacetate (Kelnor)
51
Q

Pregnanes

A

MPA, Megace

52
Q

Gonanes

A

Levonorgestrel (Seasonale)

Norgestrel (Ovral)

53
Q

Gonane derivatives (3rd gen)

A

Gestodene
Desogestrel (Kariva)
Norgestimate (OrthoCyclen)
Etenogestrel (NuvaRing, Implanon)

54
Q

Non-ethylated estranes

A

Drosperinone: progestin analogue of spironolactone; high affinity for the MC receptor and anti-androgenic activity

55
Q

Relative progestin potency

A

Gestodene > Levonorgestrel > Norgestimate > Desogestrel > NE > NEA > Drosperinone > MPA & Megace
*Most potent on primed endometrium = levonorgestrel

56
Q

Component that determines efficacy of OCPs

A

Progestin dose (inhibits LH surge, thickens mucus)

57
Q

Emergency contraception options (4)

A

Levonorgestrel: 0.75mg given twice 12h apart or in combined single dose (1.5mg)
Mifepristone: 600mg single dose, same efficacy/SE as levonorgestrel
Ullipristal: 30mg single dose, slightly more effective and similar SE to levonorgestrel
ParaGard: up to 5-10d after unprotected intercourse, failure rate as low as 0.1%

58
Q

Aromatase inhibitors SEs

A

Lower risk VTE, uteirne ca, hot flashes and bleeding than tamoxifen
Higher risk fracture and joint pain/stiffness, vaginal dryness

59
Q

Androgen receptor forms

A

A (shorter) and B (full length)

60
Q

Androgen receptor location

A

Xq11-12 (only steroid receptor on X chromosome)

61
Q

Reason for Androgen and Progesterone receptor cross reactivity

A

Similar steroid binding

62
Q

Androgen receptor mutation diseases (2)

A

AIS (similar presentation to 17-B HSD (type 3) deficiency

Kennedy’s disease (X-linked spinobulbar muscular atrophy)

63
Q

Flutamide

A

Nonsteroidal androgen receptor antagonist, can cause severe hepatotoxicity; teratogenic

64
Q

CPA

A

17-α-OHP derivative with potent progestational activity that inhibits gonadotropin secretion, competes with DHT for binding to AR and reduces serum LH and ovarian androgen concentrations, shares similar pharmacological profile to RU486 (mifepristone)

65
Q

Spironolactone

A

Aldosterone and androgen receptor antagonist structurally similar to progestins, competes with DHT for binding to AR and inhibits enzymes involved in androgen biosynthesis, can increase potassium

66
Q

Finasteride

A

Inhibits type 2 5α-reductase, enzyme converting T to DHT, only partial inhibitory effect when used for hirsutism because enhanced 5alpha reductase activity involves both type 1 (skin) and type 2 (reproductive tissues) enzymes

67
Q

Danazol

A

isoxazol derivative of 17α-ethinyl testosterone
o Mechanism of action:
• Weak-moderate binding to androgen receptor (also weak binding to PR and ER=least)
• Inhibits the midcycle urinary LH surge and induces a chronic anovulatory state
• Inhibits a number of steroidogenic enzymes (by inhibiting ovarian steroidogenesis)
• Increases free testosterone levels (by displacing from SHBG)
• Decreases serum estrogen levels
o Side effects: weight gain, acne, hirsutism, fluid retention, fatigue, reduced breast size, oily skin, atrophic vaginitis, hot flashes, muscle cramps, emotional lability, can irreversible deepen the voice, unfavorable lipid profile changes (total cholesterol and LDL increased, HDL lowered)
o Associated with virilization of female fetus in utero
o First drug approved for treatment of endometriosis in the United States

68
Q

DHEA-S source

A

100% adrenal – [3-20 mg/day]

69
Q

DHEA source

A

50% adrenal, 20% ovary, 30% peripheral conversion of DHEA-S – [6-8 mg/day]

70
Q

Androstenedione source

A

50% ovary, 50% adrenal – [1.5-6 mg/day]

71
Q

Androgen potency

A

DHT (higher affinity/slower dissociation from AR)>Testosterone>Androstenedione>DHEA-S

72
Q

Testosterone source

A

50% from peripheral conversion of androstenedione, 25% adrenal, 25% ovary

73
Q

Most abundant circulating androgen

A

Testosterone (DHT is formed intracellularly)

74
Q

Measuring Peripheral Androgen Activity

A

 3α-androstanediol glucuronide is peripheral metabolite of DHT
 Marker of target tissue cellular activity; 3AG correlates w/ 5α reductase activity in skin
 BUT, 3AG also reflects hepatic conjugation activity, and impact of precursors (androstenedione and T) derived from adrenal gland – not just from peripheral sources
 3AG is not SOLELY a measure of cutaneous androgen metabolism

75
Q

Insulin/IGF-1 Receptors

A

Grossly elevated insulin levels stimulate ovarian androgen production in theca cells via insulin, IGF-1 and hybrid receptors

76
Q

Adrenal zonas

A

Zona glomerulosa: produces mineralocorticoids
Zona fasciculata: produces glucocorticoids
Zona reticularis: produces sex steroids

77
Q

Half life hCG

78
Q

Half life FSH

79
Q

Half life LH

A

20 minutes

80
Q

Half life GnRH

A

2-3 minutes

81
Q

SHBG

A

Contains single binding site for androgens and estrogens (even though homodimer composed of two monomers)
Dimerization is believed necessary to form single steroid binding site

82
Q

SHBG increased by…

A

Estrogen, pregnancy, hyperthyroidism

83
Q

SHBG decreased by…

A

Androgens, corticosteroids/anabolic steroids, GH, insulin/IGF1, obesity/GH, menopause

84
Q

SHBG affinity of hormones (% bound)

A 
o	Testosterone (70)
o	Estrogen (70)
o	DHT (30)
o	DHEA (8)
o	Androstenedione (8)
o	Progesterone (1)

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