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MCP Unit 6 > Steroid Hormones and Vitamin D > Flashcards

Steroid Hormones and Vitamin D Flashcards

1
Q

basics

A
  • cholesterol is the precursor to all classes of steroid hormones:
    1. glucocorticoids
    2. mineralcorticoids
    3. sex hormones
  • synthesis and secretion occurs in many organs
    1. adrenal cortex-cortisol, aldosterone, androgens
    2. ovaries and placenta
    3. testes
  • travel in the blood from point of syn to target using nonspecific and specific carrier proteins
  • once reaching target, enters through PM and binds receptor in cytosol or nucleus
  • receptor binds the hormone and DNA- results in altered transcription
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2
Q

synthesis of steroid hormones

A
  • shortening of hydrocarbon chain of cholesterol and hydroxylating the steroid nucleus
  • rate limiting step is first one- cholesterol to 21C pregnenolone
  • catalyzed by cholesterol side chain cleavage enzyme
  • cytochrome p450 mixed function oxidase locatd on the inner mitochondrial membrane, requires NADPH and oxygen
  • cholesterol in the cell moves to the mito outer membrane and then inner, this is mediated by StAR
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3
Q

congenital adrenal hyperplasias

A
  • pregnenolone is precursor for all steroid hormones
  • oxidized and isomerized to progesterone
  • then further modified by hydroxylation reactions in mito and ER
  • primarily cyto p450 proteins
  • defect in any steps can cause several diminished products at later steps and build up of substrates
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4
Q

3-B-hydroxysteroid dehydrogenase deficiency

A
  • progenolone to progesterone
  • no glucocorticoids, mineralocorticoids, active androgens or estrogens
  • salt excretion in urine
  • female like genitalia
  • AR with incidence of 1/10,000
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5
Q

17-a-hydroxylase deficiency

A
  • progesterone to 17-a-hydroxyprogesterone
  • no sex hormones or cortisol
  • increased production of mineralcorticoids, causing sodium and fluid retention and hypertension
  • female like genitalia
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6
Q

21-a-hydroxylase deficiency

A

-progesterone to 11-deoxycorticosterone
-also 17-a-hydroxyprogesterone to 11-deoxycortisol
-most common form of CAH
-partial and complete deficiencies known
-mineralcorticoids and glucocorticoids absent in salt wasting classic form or deficient in non-classic form
-overproduction of androgens, leading to masculinization of external genitalia in females and early virilization in males
Hypotension

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7
Q

11-B1-hydroxylase deficiency

A
  • 11-deoxycorticosterone and 11-deoxycortisol to aldosterone and cortisol
  • decrease in serum cortisol, aldosterone, corticosterone
  • increased production of deoxycorticosterone causes fluid retention because the hormone suppresses renin-low renin HTN
  • overproduction of agdrogens-masculinization and early virulization
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8
Q

secretion of adrenal cortical steroid hormones

A
  • hormones secreted from their tissue of origin in response to hormonal signals
  • corticosteroids and androgens are produced in different parts of adrenal cortex
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9
Q

cortisol

A
  • produced in zona fasciculata of the adrenal cortex
  • its production and secretion is controlled by hypothal
  • stress–>corticotropin releasing hormone–>anterior lobe pit (thru caps)–>induces production and secretion of ACTH–>adrenal cortex synthesizes and secretes cortisol–>stimulates gluconeo and IF and immune responses
  • neg feedback from cortisol
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10
Q

role of ACTH

A
  • binds to Gs-increase cAMP and PKA
  • activates lipase that converts CE to chol and StAR, so chol moves to inner mito membrane
  • converted to pregnenolone
  • pregnenolone returned to cytosol
  • converted to progesterone
  • two ER membrane located hydroxylation steps catalyzed by CYP17 and 21- progesterone to 11-deoxycortisol
  • returned to inner mito membrane- CYP11B1 catalyzes B hydroxylation at C21, yields cortisol which can exit cell
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11
Q

functions of aldosterone

A
  • produced in outer layer of adrenal cortex-zona glomerulosa
  • stimulated by a decrease in plasma Na/K ratio and by angiotensin II
  • angiotensin II binds to G protein and activates PIP2 pathway (Gq), IP3, DAG, PKC, calcium
  • aldosterones effect on kidney tubules
  • enhances Na and water uptake and K efflux
  • increases BP
  • ACE inhibitors used to treat renin dependent hypertension
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12
Q

angiotensin II

A
  • peptide hormone (8)
  • produced by cleavage of angiotensin I (10) by angiotensin converting enzyme (ACE)
  • angiotensin I produced by cleavage of angiotensinogen, inactive precursor secreted by liver
  • cleaved by renin-proteolytic enzyme from kidneys

**renin cleaves angiotensinogen to angiotensin I–>ACE cleaves I to II

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13
Q

sex hormones

A
  • zona reticularis (inner) and middle layers

- adrenal androgens (androsterone and androstenedione) are converted to testosterone and estrogen in peripheral tissues

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14
Q

testes/ovaries

A
  • synthesize hormones required for sexual differentiation and reproduction
  • GRH (hypothal) stimulates ant pit (blood) to release LH and FSH
  • LH and FSH binds to Gs
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15
Q

LH

A

-testes to produce testosterone and ovaries to produce estrogens and progesterones

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16
Q

FSH

A

regulates growth of ovarian follicles and stimulates spermatogenesis

17
Q

estrogens

A
  • produced from androstenedione and then testosterone
  • via aromatase
  • aromatase inhibitors used for hormone positive breast cancer in post menopausal women
18
Q

steroid hormone at molecular level

A
  • can cross PM because hydrophobic enough
  • bind to cytoplasmic or nuclear receptor
  • ligand bound receptor enters nucleus if not already there
  • once in nucleus, complex dimerizes and binds to hormone response element on DNA with the help of co-activator proteins
  • HRE is in promoter or enhancer for genes responsive to the hormone
  • coordinated regulation of genes
  • if co-activator is present, mRNA is increased
  • can also decrease transcription with help of co-repressors
  • binding of ligand causes a change in the conformation of the receptor, and exposes a DNA binding domain
  • complex associates with DNA through a zinc finger motif
  • super family of receptors binds steroid hormones, thyroid hormone, retinoic acid and vitamin D
19
Q

further metabolism and secretion of steroid hormones

A
  • typically converted into inactive excretion products in the liver
  • reactions involved include reduction of unsaturated bonds and additional OH groups
  • conjugation with glucuronic acid or sulfate makes excretion products more water soluble
  • 20-30% of these metabolites are secreted into the bile and excreted in feces
  • remainder are released into the blood and filtered in kidneys
  • all excretion products are water soluble and don’t need protein carriers
20
Q

vitamin D basics

A
  • group of sterols that function like hormones
  • active molecule (1,25 diOH-D3, cacitriol) binds to receptor proteins in the cell
  • ligand receptor complex interacts with DNA in a manner similar to steroid hormones
  • regulates plasma levels of calcium and phosphorous
21
Q

endogenous source of vitamin D

A
  • 7-dehydrocholesterol
  • intermediate in cholesterol synthesis
  • converted to cholecalciferol (D3) in dermis and epidermis when we are exposed to sunlight
  • cholecalciferol transported to liver while bound to a vitamin D binding protein
22
Q

exogenous source of vitamin D

A
  • erogocalciferol (D2) which is found in plant
  • cholecalciferol (D3) in animal tissues
  • preformed vitamin D
  • dietary vitamin D is packaged into chylomicrons
  • supplementation is a dietary requirement in individuals with limited exposure to sunlight
23
Q

inactive to active vitamin D

A
  • D2,3 not active on their own
  • converted in vivo to 1,25-diOH-d3 by 2 reactions
  • first OH added in liver by 25-hydroylase- give 25-hydroxycholecalciferol, (25-OH-D3 or calcidiol)
  • major form of vitamin D in plasma and major storage form
  • further hydroxylated at 1 position by 25-OH-D3-1 hydroxylase (calcidiol-1-hydroxylase)
  • in kidney
  • forms 1,25-diOH-D3
  • both hydroxylases are cyto p450 proteins
24
Q

regulation of 25-OH-D3-1 hydroxylase

A
  • increased directly by low plasma phosphate and indirectly by low plasma calcium
  • low calcium–>PTH–>upregulates hydroxylase
  • elevated levels of calcitriol inhibits hydroxylase and expression of PTH
25
Q

regulation of plasma calcium levels by calcitriol

A

-low plasma calcium–> increased PTH–>increased calcitrol–>inc calcium mobilization from bone–>increased renal absorption of calcium–>decreased renal excretion of calcium–>increased absorption from intestine–>increased plasma calcium

26
Q

intestinal calcium absorption

A
  • calcitrol stimulates absorption
  • enters cell and binds to vitamin D receptor (VDR) in cytoplasm
  • VDR complex enters nucleus, forms heterodimer with retinoid-X receptor (RXR) and binds coactivators
  • complex recognizes VDRE in promotor/regulatory element of gene
  • can enhance or diminish cell type specific transcripts and influence expression of proteins
27
Q

VDRE

A
  • vitamin d response element in DNA
  • two hexameric nucleotide half sites separated by 3 base pairs
  • two half sites accommodate VDR-RXR heterodimer
28
Q

calbindin-D9K

A
  • in enterocytes
  • mediates transport of calcium across apical side of cell
  • TRPV5 allows entry of calcium into epithelial cell
  • transport across enterocyte cytoplasm is rate limiting- calbindin increases amount of calcium crossing cell without raising the free concentration
29
Q

vitamin D, calcium, bones

A
  • low calcium increases calcitriol via PTH
  • causes increased calcium absorption, decreased excretion, and increased demineralization
  • high calcium stops PTH
  • decreased PTH leads to more 24,25-diOH-D3 instead of 1,25 (decreased PTH decreases calcitriol)
  • causes increase in calcitonin
  • stops demineralization and increases excretion
  • deficient D means demineralization of bone
  • too much vitamin D can also cause demineralization
30
Q

vitamin D requirements

A
  • fatty fish, liver, egg yolkds
  • measure calcidiol
  • <30 is deficiency-rickets/osteomalacia
  • 30-50 adequate
  • over 50 to 125 ok
  • more than 125 could be detrimental
31
Q

vitamin D deficiency

A
  • rickets
  • osteomalacia
  • soft and pliable vs hurting ones already formed-fractures
32
Q

renal osteodystrophy

A
  • chronic kidney disease causes decreased synthesis of active vitamin D and increased retention of phophate
  • hypocalcemia aid hyperphosphatemia
  • low calcium increases PTH and demineralization
  • trt is supplement with calcitriol and reduce phosphate
33
Q

hyperthyroidism

A
  • lack of PTH cause hypocalcemia and hyperphosphatemia

- treated with calcium and calcitriol

34
Q

vitamin D toxicity

A
  • fat soluble-stored and slowly metabolized
  • excessive-loss of appetite, nausea, thirst, stupor
  • enhanced calcium absorption and bone resorption results in hypercalcemia which leads to deposits in arteries and kidneys
  • UL is 4000 IU/day for 9 years and older
  • *see slide 9

MCP Unit 6 (9 decks)

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