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NPB 130 > M1 > Flashcards

M1 Flashcards

1
Q

classes of hormones

A
  • peptides: small mol of AA
    • nonapeptides: 9 AA
    • decapeptides: 10 AA
  • proteins: more complexity ➔ made from DNA via txl/tsl
    • TSH, FSH, LH, insulin, glucagon, PRL
  • monoamines: made from AA tyrosine ➔ terminal amine + aromatic ring
    • NE, EP, dopamine
  • steroids: made from CHO
    • hydrophobic
    • intracellular recdeptors
    • estradiol, testosterone, progesterone, cortisol, aldosterone
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2
Q

hormone transport

A

hydrophilic hormones

  • water soluble ➔ easy to travel in blood
  • cell-membrane receptors

hydrophobic hormones

  • not water soluble ∴ must be bound to specific carriers/transporters to travel through blood
    • globulins
    • SHBG, TBG, albumin (most abundant)
  • intracellular receptors
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3
Q

hormone receptors

A

cell membrane receptors

  • GPCRs: 7 transmembrane passes
    • G-protein is closely associated but not bound
    • binding always extracellular
    • binding causes conformational changes
    • activates second messengers
  • RTK receptor tyrosine-kinase (insulin)
  • cytokine receptors (prolactin, GH)

intracellular receptors ➔ nuclear receptor superfamily

  • steroid receptor family form homodimers & are located in cytoplasm
    • corticoid receptor (adrenal gland hormones)
    • androgen receptor
    • progesterone receptor
  • thyroid receptor family form heterodimers w/ retinoic acid receptor & are located in nucleus
    • estrogen receptor (hybrid ➔ can form homo & heterodimers)
    • Vit D receptor
    • thyroid receptor
    • retinoid acid receptor
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4
Q

GPCR pathways

A

second messenger cAMP

  • Gs ⍺ subunit = functional
  • β & 𝛾 subunits = regulatory
  • inactive when bound to β & 𝛾 subunits
  • adenylyl cyclase converts ATP ➔ cAMP
  • cAMP activates PKA
    1. short-term effects: phosphorylates substrates outside nucleus
    2. long-term effects: PKA crosses nuclear envelope & finds & activates CREB to find CRE (cAMP response element = short sequences/regions of DNA w/ complementary portions for binding & txr/tsl)
  • most efficient: short-term available for immediate use & synthesize more for storage for immediate release upon next signal
  • ACTH, FSH

second messenger IP3 & Ca

  • Gq ⍺ subunit
  • phospholipase C converts PIP2 ➔ IP3 & DAG
    1. IP3 released in cytoplasm & travels to ER where Ca is stored ➔ mobilizes intracellular Ca
    2. Ca activates calmodulin (CaM) ➔ activates CaM kinase
    3. DAG stays in membrane & activates PKC
  • GnRH
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5
Q

second messenger cAMP

A
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6
Q

second messenger IP3 & Ca

A
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7
Q

nuclear receptor superfamily

A
  • main mechanism of action for hydrophobic hormones that bind to intracellular receptors is via transcription/translation ∴ longer response
  • nuclear receptor hormones diffuse through PM

steroid receptor family form homodimers & are located in cytoplasm

  • corticoid receptor
  • androgen receptor
  • progesterone receptor

thyroid family receptors form heterodimers w/ retinoic acid & are located in nucleus

  • estrogen receptor (hybrid ➔ can form both homo & heterodimers)
  • vit D receptors
  • thyroid receptors
  • retinoic acid receptors
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8
Q

nuclear receptor action

A

steroid receptor

  1. steroid diffuses through PM
  2. receptor held together by heat shock protein (HSP) ➔ “chaperone” stabilizing protein
  3. HSP dissociates when steroid hormone binds to receptor
  4. receptor carries into nucleus & finds to & binds HRE

thyroid receptor: hormone is carried by carrier protein into nucleus b/c receptor is already bound to HRE in DNA

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9
Q

neurophypophyseal neurons

A

PVN: paraventricular nucleus contains magnocellular & parvocellular neurons

  • AVP
  • OT
  • (CRH - part of parvocellular/adenohypophysis sysyem)

&

SON: supraoptic nucleus contains only magnocellular neurons

  • 80-90% produces AVP
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10
Q

hypophyseotropic neurons

A

contain parvocellular neurons

Arc: arcuate nucleus

&

POA: pre-optic nucleus

PVN: paraventricular nucleus (contains both magnocellular & parvocellular)

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11
Q

infundibulum

A

anatomical stalk connecting hypothalamus & pituitary gland

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12
Q

hypothalamamic hypophyseal tract

A

bundle of magnocellular axons from hypothalamus to neurohypophysis

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13
Q

median eminance

A

functional connection stalk btwn hypothalamus & adenohypophysis

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14
Q

hypophyseal portal system

A

capillary bed where parvocellular neurons release hormones to reach adenohypophysis

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15
Q

magnocellular neurons

A
  • larger cell bodies
  • longer axon projections that extend to the neurohypophysis
  • AP opens Ca v-gated channels ➔ Ca influx facilitates fusion of hormone vesicles with PM to release hormone
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16
Q

parvocellular neurons

A
  • smaller cell body
  • short axon projections that terminate in the hypophyseal portal system
  • secrete hypophysiotropic hormones that regulate secretion of adenohypophysis hormones
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17
Q

neurohypophysis

A

posterior pituitary

  • where magnocellular neurons from PVN & SON end & release hormones
  • glandular portion
  • secretion of 2 nonapeptides: vasopressin (AVP) & oxytocin (OT)
    • vasopressin = water control ➔ ↑ water reabsorption in kidneys (also regulates BP but same effect)
    • oxytocin = milk release from mammary glands, contractions, & maternal behaviors
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18
Q

adenohypophysis

A

anterior pituitary

  • cellular portion
  • somatotrophs secrete GH
  • lactotrophs secrete PRL
  • thyrotrophs secrete TSH
  • gonadotrophs secrete FSH & LH
  • corticotrophs secrete ACTH
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19
Q

pineal gland

A
  • tryptophan ➔ serotonin ➔ melatonin ➔ control of circadian rhythms & reproductive cycles for seasonal breeders
  • synthesis of melatonin in response to light/dark stimuli
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20
Q

AVP/OT precursor molecule

A
  • required for proper protein folding
  • neurophysin = critical for proper protein folding
    • propressophysin ➔ AVP + neurophysin II + glycopeptide
    • prooxyphysin ➔ OT + neurophysin I
  • precursor packed in secretory granules in Golgi apparatus & cleaved during axon transport
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21
Q

AVP fx

A

vasopressin

  • regulation of water ➔ ↑ # of aquaporins & translocation to apical membrane of principal cells of the collecting duct cells of kidney
    • most important fx
    • V2R in kidney: GPCR that uses a Gs ⍺ subunit
    • osmoreceptors in cells detect ratio of solids to liquids
      • blood osmolarity = amount of solutes in blood ➔ ↑ osmolarity (>280mOSM) = less liquid/more solutes ➔ activates osmorecdeptors
    • dehydration = main signal ➔ ↑ osmolarity & cell shrinks in size ➔ osmoreceptors can sense shrinked MP
    • short-term resposne: APQ2 translocation to apical membrane of principal cells to let water re-enter cells
    • long-term response: ↑ expression of APQ2 & APQ3 in principal cells
  • BP maintenance ➔ vasoconstriction of vessels
    • V1R = GPCR that uses a Gq ⍺ subunit
    • baroreceptors in aorta (aortic arch receptors) & carotids (carotid sinus receptors)
      • stmiulation of AVP by ↓ BP/BV
  • increase expression of ACTH receptors
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22
Q

AVP action in kidneys

A

V2R = Gs ⍺ subunit GPCR

  1. AVP binds to V2R ➔ adenylyl cyclase converts ATP ➔ cAMP ➔ activates PKA
  2. PKA phosphorylates APQ2 ➔ activates in cytosol & allows it to transport to apical membrane for water re-entry
  3. water now accumulating in cell moves through APQ3 & APQ4 channels in basolateral membrane into interstitial space
    • APQ2 & APQ3 = targets of AVP
    • APQ4 is permanent
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23
Q

diabetes insipidus

A
  • consequence of AVP deficiency
  • indiv cannot concentrate urine ➔ diluted urine, no smell or color
  • neurogenic: caused by mutations that inactivate AVP production ➔ issue is in PVN & SON nuclei
  • nephrogenic: caused by mutations in the V2R or APQ2 genes in the kidneys
  • AVP deficiency model: brattleboro rat has a genetic mutation in neurophysen II ➔ cannot fold AVP protein properly ∴ cannot synthesize AVP
    • neurogenic
    • symptoms: polyuria/polydipsia
    • urine = 80% total fluids
    • 20-30x increase in urine V than control
    • ↓↓↓ osmolarity compared to control
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24
Q

OT fx

A
  • parturition: involved in uterine contractions during stage 2 (fetal expulsion)
  • in lactation: CRITICAL for milk letdown during lactation
  • critical in parental bonding & maternal behavior
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25
Q

OT action

A

OTR = GPCR associated with Gq ⍺ subunit: phospholipase C converts PIP2 to IP3 & DAG ➔ IP3 mobilizes intracellular Ca ➔ activates CaM ➔ activates CaM kinase & DAG activates PKC to stimulate smooth muscle contraction

in parturition:

  • stage 1: fetal development
    • progesterone maintains uterine quiescence during pregnancy ➔ blocks contractions (& estrogen)
    • towards end of preg: ↑ estrogen & ↓ progesterone
    • estrogen stimulates expression of OTR in myometrium & synthesis of OT
  • stage 2: fetal expulsion
    • OT stimulates contractions in uterine fundus
    • mechanoreceptors sense pressure on cervix ➔ send signals through spinal cord to PVN & SON nuclei ➔ ⊕ feedback signals release of more OT ➔ ferguson reflex

in milk letdown:

  • OT acts on myoepithelial cells surrounding epithelial cells
  • suckling ➔ mechanoreceptors in breasts ➔ afferent signal through spinal cord ➔ stimulation of magnocellular neurons for pulsatile OT release ➔ pumping action in alveoli ➔ maximum secretion of milk
  • w/out OT: cannot secrete milk ➔ no other hormone stimulates myoepithelial cell contraction in alveoli
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26
Q

all steroids come from ___________ via ___________

A

CHO via steroidogenesis

  • steroid skeleton = 3 cyclohexane rings + 1 cyclopentane ring
  • steroidogenesis involves changes in hydroxylation & removing C
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27
Q

CHO

A
  • CHO biosynthesis: acetyl-CoA + acetoacetyl-CoA
  • maintains fluidity of PM
  • precursor mol for all steroid hormones
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28
Q

main source/site of CHO synthesis

A
  • hepatocytes in liver ➔ de novo sunthesis
  • animals must ingest ➔ cannot make enough
    • CHO in PM interacts w/ GCPR & ion pumps that have specific ion binding sites for CHO ➔ pumps are deactivated if missing/depleted
29
Q

CHO most abundant in

A

brain myelin sheaths

30
Q

CHO transport in blood

A

via LDL (low-density lipoprotein): CHO bound to the OH group of a long chain fatty acid (has CHO + other lipids)

31
Q

genes involved in steroidogenesis

A
  • there are no genes for steroids but there are genes for proteins that cleave the steroids along the pathway
  • 57 P450 enzymes ∴ 57 CYP genes
    • 7 mitochondrial
    • 50 SER
32
Q

CYP11A1 gene encoding P450scc

location:
fx:
goal:

A

located in mitochondria
fx: 10,10-desmolase
goal: CHO side chain cleavage ➔ first step in steroidogenic pathway

33
Q

CYP17A1 gene encoding protein P450c17

location:
fx:
goal:

A

locted in SER
fxs:

  • 17⍺-hydroxylase (in zona fasciculata)
  • 17,20-lyase (in zona reticulata)**

goals:

  • 17⍺-hydroxylase: pregnenolone ➔ 17⍺-hydroxypregnenolone
  • 17,20-lyase: 17⍺-hydroxypregnenolone ➔ DHEA**
34
Q

CYP21A2 gene encoding protein P450c21

location:
fx:
goal:

A

located in SER
fx: 21-hydroxylation

  • progesterone ➔ 11-deoxycorticosterone
  • 17⍺-hydroxyprogesterone ➔ 11-deoxycortisol
  • most common mutation for congenital adrenal hyperplasia (CAH)
35
Q

CYP11B1 gene encoding protein P450c11β

location:
fx:
goal:

A

located in mitochondria of ZG cells
fx: 11β-hydroxylation
goal: 11-deoxycortisol ➔ cortisol

36
Q

CYP11B2 gene encoding protein P450aldo

location:
fx:
goal:

A

located in mitochondria of zg cells
fx: 18-hydroxylation
goal: biosynthesis of aldosterone

37
Q

3β-hydroxysteroid dehydrogenase (3β-HSD)

A
  • located in SER
  • pregnenolone ➔ progesterone
  • 17𝛼-pregnenolone ➔ 17𝛼-progesterone
  • DHEA ➔ androstenedione
38
Q

17β-hydroxysteroid dehydrogenase (17β-HSD)

A
  • located in SER
  • androstenedione ➔ testosterone
  • DHEA ➔ androstenediol
39
Q

5⍺-reductase

A
  • located in SER
  • testosterone ➔ dihydrotestosterone
40
Q

sulfokinase

A
  • DHEA ➔ DHEA sulfate (DHEAS)
  • weak androgen ➔ less affinity for androgen receptor
    • works to maintain DHEAS storage
41
Q

aldosterone pathway in steroidogenesis

A

CHO
↓ CHO desmolase (CPY11A1➞ P450scc)
pregnenolone
↓ 3β-HSD
progesterone
↓ 21-hydroxylase (CYP21A2 ➞ P450c21)
11-deoxycorticosterone
↓ 11β-hydroxylase (CYP11B1 ➞ P450c11)
corticosterone
↓ aldosterone synthase (CYP11B2 ➞ P450aldo)
aldosterone**

42
Q

cortisol pathway in steroidogenesis

A

CHO
↓ CHO desmolase (CPY11A1 ➞ P450scc)
pregnenolone
↓ 17𝛼-hydroxylase (CYP17A1 ➞ P450c17)
17⍺-hydroxypregnenolone
↓ 3β-HSD
17⍺-hydroxyprogesterone
↓ 21-hydroxylase (CYP21A2 ➞ P45c21)
11-deoxycortisol
↓ 11β-hydroxylase (CYP11B1 ➞ P450c11)
cortisol**

43
Q

androgen pathway in steroidogenesis

A

CHO
↓ CHO desmolase (CPY11A1 ➞ P450scc)
pregnenolone
↓ 17𝛼-hydroxylase (CYP17A1 ➞ P450c17)
17⍺-hydroxypregnenolone
↓ 17,20-lyase (CYP17A1 ➞ P450c17)
DHEA
↓ 3β-HSD
androstenedione
↓ 17β-HSD
testosterone**

44
Q

zones of the adrenal gland

A

**cortex: steroid hormones ➔ derived from mesoderm of abdominal wall

  • zona glomerulosa ➔ aldosterone synthesis
    • mineralocorticoids ➔ aldosterone
      • “minerals” ➔ regulating mineral balance (salt) in kidneys
    • virtually no MC2R ➔ non-responsive to ACTH
  • zona fasciculata ➔ glucocorticoids ➔ cortisol synthesis
    • cortisol fx: ↑ glucose levels in blood via gluconeogenesis in liver
    • majority of cortex
    • most responsive to ACTH ➔ slight hypertrophy & hyperplasia
  • zona reticularis ➔ androgen synthesis
    • dehydroepiandosterone (DHEA)
    • important for females
    • responsive to ACTH

medulla: non-HPA hormones

  • epinephrine
  • norepinephrine
  • derived from neuroectoderm: ANS/SNS**
45
Q

CHO uptake & initiation of steroidogenic pathway

A
  1. start with LDL
  2. internalized by cell via LDL receptor
  3. inside cell: LDLR + LDL is endocytosed ➔ receptor is reparated from the LDL in the endosome & LDL (CHO ester = bound to fatty acid) is hydrolyzed by CHO esterase that releases free CHO
  4. LDLR recyled back to PM
  5. StAR protein finds free CHO & carries to mitochondria where steroidogenesis begins
  6. steroidogenesis starts in mitochondria ➔ goes to SER ➔ back to mitochondria for adrenal hormone synthesis**
46
Q

parvocellular hypothalamaic nuclei

A

PVN

  • CRH ➔ corticotroph cells secrete ACTH ➔ act on adrenal gland
  • TRH ➔ thyrotroph cells secrete TSH ➔ act on thyroid gland
  • AVP produced by magnocellular neurons & secreted by neurohypophysis to regulate water & BP & also produced by parvocellular neurons as a 2º stimulatory signal for ACTH release ➔ maximizes response**

ARC

  • GnRH ➔ gonadotrophs cells secrete LH & FSH ➔ act on gonads
  • GHRH ➔ somatotroph cells secrete GH ➔ act on liver
  • SST: somatostatin ➔ inhibitory: ⊖ regulator of GH
  • dopamine ➔ inhibitory: ⊖ regulator of PRL

POA

  • GnRH

VIP: prolactin-releasing factor ➔ lactotroph cells secrete PRL

47
Q

adenohypophysis hormone main fxs

A

positive actions ➔ stimulate glands

ACTH:

  • synthesis of adrenal hormones
  • ↑ in adrenal weight (due to ↑ activity)

PRL

  • mammary growth
  • milk synthesis
  • thermoregulation
  • behavioral
  • immune-related

TSH

  • synthesis of TH
  • thyroid weight (active cells enlarge)

FSH

  • follicle growth
  • spermatogenesis
  • estradiol production ➔ conversion of androgens to estrogens

GH

  • tissue growth
  • metabolic effects

LH

  • ovulation
  • testosterone production
48
Q

ACTH action

A
  • ACTHR = MC2R: melanocortin 2 receptor
    • expressed in zona fasciculata & zona reticularis
  • effects
    • ↑ glucocorticoids (main response)
    • ↑ DHEA
    • ↑ adrenal weight via hypertrophy (increased secretory activity ➔ cells swell) & hyperplasia
    • ↑ medullary hyperplasia ➔ ↑ release of EPI & NEPI
    • ↑ expression & translocation of LDLR to membrane to facilitate LDL internalization of CHO for steroidogenesis
    • intracellular activation by PKA:
      • CHO esterase
      • Star activated
      • P450scc
    • ↑ gene expression of CHO esterase, StAR protein, & P450scc**
49
Q

ACTH response to hypoglycemia

A
  1. stimulates PVN in hypothalamus to release CRH ➔ enters portal system
  2. stimulates corticotrophs in adenohypophysis to release ACTH into systemic circulation
  3. stimulates adrenal gland to produce cortisol in the zona fascicularis
  4. stimulates liver gluconeogenesis
  • prolonged stress response surpasses circadian rhythm
  • prior high-dose synthetic glucocorticoid administration abolishes stress response
  • ↑↑ adrenal hormone levels act as negative feedback to HPA axis**
50
Q

ACTH precursor

A

proopiomelanocortin (POMC)

  • mol have diff biological activity depending on cleavage location
    • 𝛼MSH ➔ food intake, metabolic rate
    • β-endorphin ➔ endogenous opioid
  • response depends on site of hormone synthesis & receptor
    • MC1R in melanocytes & leukocytes of skin ➔ stimulates melanin prod
      • prevents/limits further UV penetration
      • repairs DNA damage
    • MC2R for ATCH in adrenal cortex ➔ cortisol synthesis
    • MC3R in CNS ➔ feed intake regulation
51
Q

congenital adrenal hyperplasia (CAH)

A
  • lack of cortisol prod during fetal development ➔ lack of ⊖ feedback for HPA axis
  • results from a defficiency in an enzyme in the cortisol pathway (mutations in the CYP21A2 gene that encodes P450c21 that converts progesterone ➔ 11-deoxycorticosterone & 17⍺-hydroxyprogesterone ➔ 11-deoxycortisol)
  • excess of ACTH & overstimulation of adrenal gland cause:
    1. adrenal hyperplasia
    2. excess prod of adrenal androgens ➔ pathway will be overactivated but the only direction it can go is towards androgens (masculinization = problematic for females)
52
Q

systemic effects of cortisol excess

A

brain:

  • depression
  • psychosis

endocrine:

  • ↓ TSH, LH, & FSH release
  • ↓ GH secretion

eye: glaucoma

carbohydrate/lipid metabolism:

  • ↑ hepatic glycogen deposition
  • ↑ peripheral insulin resistance
  • ↑ gluconeogenesis
  • ↑ free fatty acid production
  • overall diabetogenic effect

adipose tissue distribution: promotes visceral obesity

bone & calcium metabolism:

  • ↓ bone formation
  • ↓ bone mass & osteoporosis

skin/muscle/connective tissue:

  • protein catabolism/collagen breakdown
  • skin thinning
  • muscular atrophy

immune system:

  • anti-inflammatory action
  • immunosuppressant

growth & development: ↓ linear growth

cardiovascular/renal:

  • salt & water retention
  • hypertension

GI tract: peptic ulcers

53
Q

glucocorticoid regulation of BG

A
  • most tissues in body express glucocorticoid receptor
  • glucocorticoid effects counteract insulin: insulin inserts glucose channels to facilitate glucose uptake by tissues
  • cortisol ↑ BG by inhibiting uptake in peripheral tissues & by stimulating gluconeogenesis
    • “glucose sparing effect”
    • catabolic effects to break apart gluconeogenesis substrates
      • muscle: stimulates myostatin ➔ proteolysis to release AA
      • adipose tissue: stimulates hormone-sensitive lipase (HSL) ➔ lipolysis to release FA & glycerides
      • liver: stimulates PEPCK & glucose-6-phosphatase: gluconeogenic enzymes**
54
Q

targets of cortisol in BG in homeostasis

A
  • stimulates gluconeogenesis
    • glucose-6-phosphatase
    • phosphoenolpyruvate carboxykinase (PEPCK)
  • stimulates glycogen synthase
  • inhibits glycogen phosphorylase
  • Activates lipolysis: hormone-sensitive lipase (HSL) breaks down fatty acids
  • ↓ protein synthesis
  • stimulates myostatin to break down muscle fibers**
55
Q

systemic effects of chronic synthetic glucocorticoids (hyperadrenocorticism)

A
  • ↑
    • PEPCK, myostatin, lipase
    • circulating AA
    • BG (↑ 50%)
  • ↓
    • body weight ➔ change in the pattern of fat distribution: visceral fat accumulation
    • muscle mass
    • endogenous cortisol
  • removing synthetic glucocorticoid supplementation could send indiv into hypoadrenocorticism b/c HPA axis was strongly inhibited by ⊖ feedback ➔ system doesn’t resume as quickly as rx is halted
56
Q

GCR action

A

held together by heat shock protein (HSP) until GC binds, then dissociates

57
Q

clinical uses of glucocorticoids

A
  1. allergic dermatitis
  2. transplant recipients
  3. inflammatory diseases ➔ potent inhibitors of immune system
58
Q

inflammatory response

A
  • inflammation = results of 1st line of defense (innate)
  • initiated on site of antigen contact
  • clinical signs:
    • swelling ➔ edema from blood
    • redness
    • heat ➔ tons of metabolic activity generates heat
    • pain
    • tumor ➔ enlarged site b/c extra cells migrate to area
    • loss of fx ➔ tissue busy fighting injury
59
Q

regulation of immune system by glucocorticoids

A

2 levels of immune defense:
* innate - 1st line
* antigen presenting cells ➔ macrophages, dendritic cells, neutrophils
* phagocytosis of antigens at site of injury
* antigen processing & presentation
* production of pro-inflammatory cytokines: interleukins (IL) & tumor necrosis factors (TNF)

  • acquired - 2nd line
    • attract other immune cells
    • build immune memory
  • steroids act at beginning of inflammatory cascade to block entire pathway
  • NSAIDs block specific parts of the pathway but not other ➔ attenuate & minimize response but don’t completely stop it
60
Q

aMSH is found in

A
  • intermediary lobe of pituitary
  • Arc
  • keratinocytes (MC1R)
61
Q
A

A: GnRH (females)
B: CRH + AVP
C: TSH
D: dopamine
E: GnRH
F: GHRH
G: SST (somatostatin)

62
Q
A

A: corticotrophs
B: thyrotrophs
C: gonadotrophs
D: somatotrophs
E: lactotrophs

63
Q
A

A: ACTH
B: TSH
C: PRL
D/E: LH & FSH
F: GH

64
Q

parvocellular neurons

A

A: POA
B: PVN
C: Arc

65
Q

what hormone stimulates OT receptors & OT

A

estrogen

66
Q

precursor for oxytocin

A

prooxyphysin

67
Q

precursor for vasopressin

A

propressophysen (neurophysen II + glycopeptide)

68
Q
A

glomerulosa

hormone B: pregnenolone
enzyme E: 3β-HSD
hormone C: progesterone
enzyme G: P450c21
enzyme H: P450c11
enzyme J: P450aldo

fasciculata

  • enzyme B: P450c17
  • hormone D: 17⍺-hydroxypregnenolone
  • enzyme E: 3β-HSD
  • enzyme H: P450c11
  • hormone O: cortisol

reticularis

  • enzyme C: 17,20-lyase
  • hormone F: DHEA
  • enzyme F: sulfokinase
  • hormone J: DHEAS
  • enzyme E: 3β-HSD
  • hormone H: androstinedione
  • enzyme D: 17β-HSD
69
Q
A
  • hormone B: pregnenolone
  • enzyme E: 3β-HSD
  • hormone C: progesterone
  • enzyme G: P450c21
  • hormone K: 11-deoxycorticosterone
  • enzyme H: P450c11
  • hormone M: corticosterone
  • enzyme J: P450aldo
  • hormone N: aldosterone
  • enzyme B: P450c17 ➞ 17⍺-hydroxylase
  • hormone D: 17⍺-hydroxyprenenolone
  • hormone E: 17⍺-hydroxyprogesterone
  • hormone L: 11-deoxycortisol
  • hormone O: cortisol
  • enzyme C: P450c17 ➞ 17,20-lyase
  • hormone F: DHEA
  • hormone H: androstinedione
  • enzyme D: 17β-HSD
  • hormone I: testosterone
  • hormone G: androstinediol

NPB 130 (5 decks)

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