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Biochemistry > Block 3 Cholesterol Derivatives > Flashcards

Block 3 Cholesterol Derivatives Flashcards

1
Q

In what form is cholesterol excreted?

A

Bile acids and salts, mechanism: metabolic product of cholesterol or solubilizer of free cholesterol excretion in bile

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2
Q

How are bile acids synthesized?

A

In liver, 15 steps requiring 4 organelles (last is perox)

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3
Q

What is the difference between the classic/neutral and alt/acidic pathway of bile acid synthesis?

A

Classic: bio-transformation of sterol nucleus occurs before side chain mods
Acidic: side chain mods before mods of sterol nuc

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4
Q

Describe the classical pathway of BA synthesis.

A

Hydroxylation in 7a position of chol B ring, catalyzed by CYP7A; inhibited by BA (major reg); then saturate 5,6 =, epimer 3b-OH to a, add OH to 12a of C ring, 3C cleave side chain, ox C24 to carboxylate

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5
Q

What is farnesyl X receptor?

A

FXR inhibits CYP7A

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6
Q

What are the primary bile acids?

A

Chalk acid and chenodeoxycholic acid (weak acids, can pass into enterocyte by passive diff)

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7
Q

What are bile salts?

A

Bile acids further conjugated by the liver (with glycine pK 4, taurine pK 2); lower pK makes salt more ionic = better emulsifying (^ amphipathic), trapped in lumen (-), active transport reabsorption

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8
Q

How are bile salts synthesized?

A

Cholic acid + ATP + CoASH -> cholyl-CoA + taurine or glycine in amide linkage -> tauro- or glyco-cholic acid

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9
Q

What are secondary bile acids?

A

Bile salts modified by bacterial flora, removal of glycine/taurine and OH at C7; less soluble, less readily reabsorbed from lumen -> excretion

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10
Q

What is enterohepatic circulation?

A

Recirculation of bile acids 10-20x/day; reabsorbed from int lumen -> liver via portal vascular system; 5% eliminated, 6-800 ml bile produced/day (1.5-4g)

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11
Q

What is bile?

A

Complex aqueous mixture with non-lipids like organic an/cations, neutral amphipaths, lipids like bile acids, chol, PLs (mainly PC)

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12
Q

What kind of receptors mediate secretion of specific bile components? How are they regulated?

A

ATP-binding cassette (ABC) family of transporters; reg by liver X receptor (LXR)

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13
Q

Which transporters secrete PLs? BAs? Chol?

A

PL: ABCB4, MDR3
BA: ABCB11
C: ABCG5/8 (same as enterocyte)

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14
Q

How is a biliary micelle formed?

A

Bile salt from ABCB11 in bile interacts with B4 and G5/8 -> micelle

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15
Q

How do bile salts affect mixed micelles?

A

Drive C and PL (makes C soluble, prevents crystals, protects cells lining biliary tree from toxic action BS) secretion, stabilize micelles

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16
Q

How are gallstones formed?

A

C/PC ratio increases from canalicular space to bile ducts to gallbladder -> C crystal; overproduction hydrophobic BS (deoxycholate), GB hypo motility, mucin hypersecretion

17
Q

How do GB hypo motility and mucin hyper secretion lead to gallstone formation?

A

GB: chol over-secretion increase resident time, allows nucleation chol -> crystal
Mucin: mucin gel matrix provides scaffold for crystal

18
Q

What is cholesterol gallstone disease called? How is it treated?

A

Cholelithiasis; tx administer chenodeoxycholic acid (may take months/y to dissolve) or surgical removal

19
Q

What are the roles of bile acids?

A

Excretion of chol, facilitate int absorption dietary TG and liposoluble vits

20
Q

What are the compensatory mechanisms against elevated chol?

A

Reduced absorption chol, increase in BA synth, reduced ability fibroblasts to synth chol

21
Q

What are the five main classes of steroid hormones?

A

Progestins, glucocorticoids, mineralocorticoids, androgens, estrogens

22
Q

Where are gluco and mineralocorticoids produced? What are the major functions? What are common examples?

A

Adrenal gland; cortisol and aldosterone; maintenance of carb metab, stress management, salt balance

23
Q

Where are progestins and estrogens produced? What are the major functions? What are common examples?

A

Ovary and placenta; progesterone, estradiol; induce secondary sex characteristics, essential for reproduction

24
Q

Where are androgens produced? Major functions? Common example?

A

Testis; testosterone; maintenance of reproductive function, secondary sex characteristics

25
Q

What 2 types of enzymes are required for conversion of chol to steroid?

A

CYP (membrane-bound, in ER or IMM) and side-chain DH (cytosol or ER)

26
Q

What is aromatase? What does it do?

A

A CYP hydroxylase, cleaves C-C bond, “aromatization” of neutral sterol A ring; converts testosterone to estradiol

27
Q

How are cortisol and cortisone interconverted?

A

Sol to sone: 11b-hydroxysteroid DH converts hydroxyl to keto (oxidase)
Sone to sol: reductase

28
Q

What are the 2 isoforms of 11b-hydroxysteroid DH?

A 
Type 1 (liver): bidirectional, potential to restore cortisone to active cortisol
Type 2 (kidney): unidirectional to inactivate cortisol to cortisone
29
Q

What are the two levels of steroid production control?

A

Acute control at level of substrate (chol) mobilization & long-term at level of gene transcription; both under control of trophic protein hormones

30
Q

What is ACTH? LH, FSH? AT-2?

A

ACTH: regulates glucocorticoid biosynthesis
LH/FSH: reg gonadal hormone biosynth
AT-2: regulates mineralocorticoid synth

31
Q

What is the first step in steroid hormone synthesis?

A

Conversion of chol to pregnenolone by side chain cleavage (P450scc); in mito, cytosolic export

32
Q

How do trophic hormones affect steroid hormone production?

A

Interact with PM receptors to form cAMP (ATP hydrolysis), activates PKA -> CE hydrolase, StAR (steroidogenic acute protein) post-tln mod; FC -> IMM via cytoskeletal proteins (to OMM) and StAR (to IMM)

33
Q

What is the limiting step in steroid synthesis?

A

Translocation of cholesterol between OMM and IMM, controlled by StAR activity

34
Q

What is lipoid congenital adrenal hyperplasia (lipoid CAH)? How is it treated?

A

Loss of fxn StAR -> large adrenals full of CE, hyponatremia and -kalemia, phenotypically female regardless of gonadal sex
Tx: mineralo- and gluco-corticoid replacement therapy

35
Q

What is vitamin D3 and D2?

A

D3: cholecalciferol (natural) produced in skin under UV light
D2: ergocalciferol formed in plants by UV irradiation (supplement in milk)

36
Q

How are D vits activated?

A

In liver, D3 hydroxylated in O2-requiring rxn -> 25-HCC

In kidney, 25-HCC hydroxylated by mito oxygenate to active 1a,25-DHCC

37
Q

Why is vit D important in Ca homeostasis? What is vitamin D intoxication?

A

Increases serum Ca by promoting int abs and stimulating release from bone; high serum Ca -> calcification soft tissues (kidney stone, bone demineralization)

Biochemistry (17 decks)

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