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Endocrine > Steroid Biosynthesis > Flashcards

Steroid Biosynthesis Flashcards

1
Q

progestins sites of synthesis, distribution, and effects

A
  • synthesized in adrenal gland, ovaries, testes
  • distributed to uterus
  • mediates implantation and maintenance of pregnancy
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2
Q

glucocorticoids sites of synthesis, distribution, and effects

A
  • synthesized in adrenal glands
  • distributed to a large number of tissues and organs
  • inc BP and Na uptake in the kidneys
  • mediates response to stress by increasing protein catabolism and gluconeogenesis and reducing inflammation
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3
Q

mineralocorticoids sites of synthesis, distribution, and effects

A
  • synthesized in adrenal glands
  • distributed to kidney tubules, colon, and parotid gland
  • increases Na/water retention, K excretion, and BP
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4
Q

estrogens sites of synthesis, distribution, and effects

A
  • synthesized in ovaries, placenta, and adipose tissue
  • distributed to primary and secondary reproductive organs
  • mediates feminization, estrous cycle, and inhibits testosterone synthesis
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5
Q

androgens sites of synthesis, distribution, and effects

A
  • synthesized in adrenal glands, ovaries, and testes
  • distributed to primary and secondary reproductive organs and muscle
  • mediates spermatogenesis, secondary male characteristics, bone maturation, and virilization
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6
Q

endocrine signaling

A

a. Long distance signaling
b. Signalbloodstreamdistant target cells
c. Freely diffusible signals
d. Long lasting (long half life in min)takes time to go thru the circulatory system to find a target cell
e. Steroids are very stable, diffusible

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7
Q

ligands

A

i. Can be proteins, small peptides, AAs derivatives, hydrophobic mcs (steroid Hs like estrogen)
ii. Even gases (NO)
iii. Main categories:
1. Small lipophilic mcs—steroid Hs
2. Water soluble mcs—hydrophilic—growth factors

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8
Q

cholesterol conversion to steroid Hs

A

a. Distal signaling mcs—steroid or peptide Hs
b. Steroids are important signaling mcs synthesized from cholesterol
c. unlike peptide Hs (which bind to their receptors on a cell’s outer surface) steroids target cells and binds to receptors in the cytoplasm that translocate to the nucleus
d. longer lasting signal due to stability and turnover rate
i. important for endocrine signaling—must travel thru the body
e. receptors are transcription factors
i. bind to signaling H and to DNA
ii. most of which have a domain that can interact in transcriptional complexes to initiate/repress gene expression
iii. steroid signaling is slow b/c it has to cause the transcription of genes

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9
Q

steroid Hs regulate:

A

i. cell growth and differentiation into specific cell types
ii. the body’s response to stress
iii. metabolism of nutrients

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10
Q

what kind of Rs do steroid Hs bind?

A

i. unlike peptide Hs (which bind to their Rs on a cell’s outer surface—steroids target cells and bind to Rs located in the cytoplasm that translocate to the nucleus
1. longer lasting signal due to stability and turnover rate

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11
Q

2 types of R

A

i. intracellular R—steroid R can have R in cytosol (estrogen)—alters gene expression in nucleus
1. small hydrophobic signaling mcs can diffuse across the cytoplasmic membrane and bind to intracellular R
ii. cell surface Rs—external domain binds ligand, transmembrane domain anchors R, cytoplasmic domain initiates signal by change in conformation
1. most signaling mcs are hydrophilic and require cell surface R

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12
Q

where do steroid Hs get the cholesterol?

A

a. synthesized from cholesterol in the SER of the adrenal cortex, ovaries, and testes
i. these tissues obtain cholesterol from:
1. circulating LDL
2. de novo synthesis from acetyl CoA
a. acetyl CoA is abuilding block for fatty acids, and if not using the citric acid cycle to generate energy, then stored as fatty acids which is material to make cholesterol
b. don’t get cholesterol this way if we are starving
c. IPP is where our small C anabolic pathways become our fatty acids and cholesterol
i. Essential for deriving anything that is cholesterol based
3. cholesterol esters stored in cytoplasmic lipid droplets

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13
Q

desmolase

A

i. synthesis of steroid Hs begins with rate limiting step catalyzed by desmolase
1. enzyme incorporates a carbonyl group on the D ring of the cholesterol and cleaves off a 6 carbon piece of its side chain to form pregnolone
2. this step must be regulated
3. this is a step where we can intervene with a drug

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14
Q

progesterone is specifically converted in a tissue specific manner to:

A
  1. aldosterone—mineralocorticoid
    a. made in the adrenal cortex (zona glomerulosa)
  2. cortisol—glucocorticoid
    a. made in the adrenal cortex (zona fasciculate)
  3. estradiol—estrogen
    a. from testosterone in ovaries
    b. minor amount in the adrenal cortex
  4. testosterone—an androgen
    a. dihydroterstosterone—more potent form found in the testes that is specific to males and has a greater effect on the Rs
    b. minor amount in adrenal cortex
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15
Q

pregnolone acts as what in signaling?

A
  1. acts as a modulator of NT signaling in the brain without being converted to other steroids
    a. effects the NMDA glutamate R—memory and learning
    b. tx thought to help in multiple neurological disorders
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16
Q

how does progesterone act for the synthesis of other progesterens

A

must be converted to progesterone for synthesis of other progesterens—utilizes enzymes 17-alpha-hydroxylase and 3-beta-hydroxysteroid dehydrogenase

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17
Q

what does mineralocorticoids affect?

A

i. affect Na/water levels in tissues

18
Q

what does glucocorticoids affect?

A

i. affect brain development
ii. affect immune function (suppression)
iii. affect glucose metabolism and fight/flight (epinephrine)
iv. have affinity for mineralocorticoid Rs and are 100 times more conc than mineralocorticoids (corr box)

19
Q

what do estrogens affect?

A

female sex characteristics

20
Q

what do androgens affect?

A

i. male sex characteristics
ii. anabolic steroids
1. synthetic forms used as performance enhancing
a. affect natural testosterone in signaling pathways

21
Q

where is demolase found and what is it needed for?

A
  1. essential for the production of pregnolone
  2. P-450 family—monooxigenase
  3. It is only found in tissues that produce steroid Hs—gonads and adrenal cortex
22
Q

adrenocorticotropic H and desmolase

A

a. secreted during stressful conditions (low blood sugar, cold, exercise)
i. From pituitary gland but turned on by corticotropin releasing H from the hypothalamus
ii. Stimulates release of cortisol from adrenal cortex
iii. Activates expression of desmolase so it takes awhile for desmolase to turn on and off
1. if you have enough cortisol around due to high ACTH, then causes weight gain, mood disorders

23
Q

luteinizing hormone and desmolase

A

i. from pituitary gland but turned on by gonadotropin releasing H (GnRH) from hypothalamus
ii. increases activity of desmolase—faster acting

24
Q

follicle stimulating H

A

i. from pituitary gland but turned on by gonadotropin releasing H (GnRH) from hypothalamus
ii. males—promotes spermatogenesis
iii. females—affects menstruation, stimulates estradiol production in ovaries and activates the enzyme aromatase

25
Q

21 hydroxylase deficiency

A
  1. common inherited defect (1/12000 live births)
    a. leads to salt wasting (hyponatremia) and hypotension due to decreased production of aldosterone, and hypoglycemia due to decreased production of cortisol
    b. in females, this deficiency causes virilism (development of male secondary characteristics) due to increased flow of intermediates into adrenal androgens
26
Q

17 alpha hydroxylase deficiency

A

a. causes a loss of cortisol as well as sex steroids
b. however, the decrease in cortisol is compensated for by increased production of corticosterone
c. problem that is far upstream so can cause a lot of problems leading to early death

27
Q

11 beta hydroxylase deficiency

A

a. cause hypertension due to the accumulation of 11 decoxycorticosterone which has mineralocorticoid activity

28
Q

where does aldosterone come from? and what are the effects?

A

a. (a mineralocorticoid)
i. adrenal cortex (zona glomerulosa)
ii. promotes the retention of Na and water in the kidneys as well as excretion of H and K
reduced levels—loss of too much salt

29
Q

Conn Syndrome*

A
  • excessive aldosterone levels

- causes inc BV, hypertension

30
Q

cortisol–where from? and what effect?

A

i. adrenal cortex (zona fasciculata)
ii. anti inflammatory and autoimmune properties
iii. stimulates the breakdown of muscle, gluconeogenesis, and glycogen synthesis

31
Q

Cushing Syndrome*

A
  • elevated levels of cortisol
    i. condition marked by the accumulation of fat on the face and trunk
    1. can be caused by increased cortisol production due to pituitary or adrenal tumors or chronic administration of corticosteroids
32
Q

cortisol in immune system

A
  1. cortisol suppression of the immune system cause immunosuppression by inhibiting both cellular and humoral immune response
  2. glucocorticoids induce the production of i-kappa(BA) inhibitory protein which helps sequester the TF nuclear factor NF-kappaB
  3. cortisol also promotes T cell apoptosis
33
Q

mineralocorticoid target tissues such as the kidney, colon, and parotid gland contain a R ….

A

that has equal affinity for both mineralocorticoids and glucocorticoids

34
Q

what enzyme metabolizes cortisol to cortisone?

A

11 beta hydroxysteroid dehydrogenase

35
Q

cortisone and mineralocorticoid R

A

a. cortisone has a much lower affinity for the mineralocorticoid R

36
Q

natural licorice

A

i. natural licorice root contains isofavones which are inhibitors of 11 beta hydroxysteroid dehydrogenase
1. consumption of real licorice can lead to hypertension due to salt retention

37
Q

DHT

A

a. the androgenic potency of testosterone is amplified by its conversion to dihydrotestosterone (DHT) mediated by the enzyme (5 alpha reductase)
i. DHT has a much higher affinity than testosterone for the androgen R
ii. Finasteride, an inhibitor 5 alpha reductase, prevents this potentiation
1. has been used to treat benign prostatic hyperplasia
2. also used to treat male pattern baldness which is caused by the action of DHT in the scalp
a. similar to the use of tamoxifen (estrogen)

38
Q

vitamin D

A

a. effects of vitamin D are attributed to its active form—calcitriol
b. technically not a steroid
i. cholesterol’s sterane structure is broken during the synthesis like steroid Hs
ii. though, vitamin D acts thru binding to a nuclear Rs and altering the expression of target genes containing vitamin D response element (VDRE) sequences
c. derived from cholesterol
d. has signaling properties like steroid Hs
e. involved in calcium absorption
f. can take up from diet and sunlight

39
Q

mechanism of vitamin D

A

i. cholecalciferol (vit D3) is the inactive form of vit D
1. produced in the skin from the photochemical cleavage of the B ring of 7 dehydrocholeterol (via UV irradiation in the skin)
2. in intestinal cells form ergocalciferol (vit D2)
ii. subsequent steps take place in both the liver and kidneys
1. cholecalciferol is first hydroxylated in the liver by 25 hydroxylase to generate 25 hydroxycholecalciferol
iii. 25 hydroxycholecalciferol is then hydroxylated in the PCT of the kidneys by 1 alpha hydroxylase
1. generates 1, 25 dihydroxycholecalciferol (calcitriol)
2. the action of 1 alpha hydroxylase is stimulated by parathyroid H (PTH) and low blood concentrations of phosphate but inhibited by calcitriol

40
Q

vitamin D signaling

A

i. calcitriol stimulates intestinal cells to:
1. increase the absorption of Ca and phosphate from the intestinal lumen
2. increase the reabsorption of Ca by kidneys
3. promote resorption of Ca from bone
a. resulting effect of calcitriol is an elevation in blood Ca and phosphate levels
i. PTH and calcitonin are peptide signals

41
Q

deficiencies of vitamin D

A

i. Inadequate dietary intake
ii. Conditions that disrupt absorption of lipids
iii. Poor functioning of the liver and kidneys
iv. Hypoparathyroidism
v. Lack of exposure to sunlight
vi. Brittle bones and deformities
1. Kids—rickets
2. Adults—osteomalacia and fractures
vii. Hypocalcemic tetany—involuntary muscle contractions due to low blood Ca

Endocrine (15 decks)

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