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Biochem Unit 2 > Lightbody Lecture 15 and 16 > Flashcards

Lightbody Lecture 15 and 16 Flashcards

1
Q

lipoprotein particles

A

Plipid, prot (apoprot), cholesterol (free and esterified), and TAG; transport lipids to periph tissues and return excess to liver; constant synth, transition, degrad, and removal from plasma; role in myo infarc, stroke, periph vasc disease, other inflam; synth in liver and intestine; heterogen in size and density; must go back to liver to be metab

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2
Q

chylomicrons

A

90% TAG, 5% cholesterol, 2% prot (largest w/lowest density)

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3
Q

VLDL

A

60% TAG, 20% chol, 5% prot; smaller and more dense than chylo

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4
Q

LDL

A

4% TAG, 50% chol, 25% prot; smaller and more dense than chylo or VLDL; Plipid single layer memb interspersed w/free chol (unesterified); apoprots are on surface (some integ, some periph); one apoB100 per LDL, encircles like belt; inner core is chol ester and TG

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5
Q

HDL

A

8% TAG, 30% chol, 33% prot; smallest and most dense

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6
Q

apolipoproteins/apoproteins

A

on lipoprot particle surface; interact w/receps on cells, det fate of LPP; activate/inhib enz’s; each has unique set of apoprots; transferred from one LPP to another; diff isoforms (some assoc w/disease (AD-apoE)

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7
Q

Apo A-I

A

most abund prot on HDL; maturation of HDL and efflux of chol from cells to HDL; bds to scavenger receps on liver cells, activates LCAT (esterifies chol to FAs)

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8
Q

Apo B 100

A

req for form of VLDL; 1o prot of LDL, acts as ligand for LDL recep (LDLR) to allow chol deliv; v large (4400 AAs)

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9
Q

Apo B 48

A

truncated form of apo B 100, synth’d in intestine and req’d for chylomicron formation; only on chylos

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10
Q

Apo CII

A

on chylos, VLDL, HDL; activates lipoprotein lipase (LPL), exchanged b/w diff lipoprot classes

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11
Q

Apo CIII

A

synth’d in liver and int, on chylos, VLDL, LDL, HDL; inv in inflam; high concs assoc w/cardiovasc disease

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12
Q

Apo E

A

synth in liver on HDL, trans to chylos and VLDL, where acts as ligand for rem chylo remnants and IDL from circul thru LDL recep or LRP recep (E2-4); may clear amyloid fr brain

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13
Q

Apo E4

A

genetic risk factor for late-onset AD; homozygote at 68y; hetero at 75; no alleles 84; E3 most common, but E4 have 20x risk of devel AD; E2 decreases risk

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14
Q

chylomicrons

A

carry dietary TAG to other tissue to be used for E or stored; syn in enterocytes, sec into blood to LPL; resulting remnant endocytosed into liver, dig into individ cmpnts

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15
Q

lipoprotein lipase (LPL)

A

on capil walls of endothel cells; hydrol TAG to FFAs (80% - other 20% goes to liver); activated by ApoCII

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16
Q

intermed density lipoprot

A

formed in VLDL breakdown; 50% returns to liver, 50% becomes LDL (loses ApoE)

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17
Q

lipoprot lipase deficiency

A

evident in infancy; pancreatitis, nausea, musc pain, fatty deposits (xanthomas); elevated chol, high triglycerides after 12h fast, normal apo CII; restrict dietary fat (<10g/d); inc carbs and prots; inc fat-sol vits; mortality b/c pancreatitis

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18
Q

ApoE and Apo B 100 bdg

A

extended form on VLDL surface, can’t bind w/recep; VLDL dec in size as TAG hydrol by LPL, /\ing conform of ApoE and B100 and allows them to bd to LDL recep as VLDL transformed to IDL

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19
Q

LDL fxn

A

derived from VLDL via IDL; has 4% TAG, 50% chol; main fxn is provide chol to periph tissue, return maj of excess to liver; 70% chol returned via LDL, rest via HDL; high assoc w/atherosclerosis, myo infarct, stroke, periph vasc disease (bad chol)

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20
Q

small, dense LDL

A

300x more likely to cause myo infarct or stroke; predictor of cardiovasc events and CAD

21
Q

HDL

A

heterogeneous gp; synth in liver, some int; reservoir for CII and E; Apo A (combines w/scavenger recep on PM of liver instead of LDLR) is most abund prot on HDL surface; picks up free chol, esterifies it, transfers to LDL (70%) or VLDL or returns direc to liver (30% via HDL); at same t, VLDL and LDL transfer TAG to HDL; raised by exercise, low wt, no smoke, no trans fat, alcohol, omega FAs, niacin

22
Q

ABCA1-ATP bdg cassette transporter

A

bds to apo-AI–>transport of free chol from cell to HDL, where esterified by LCAT

23
Q

LCAT (lecithin-chol acyl transferase)

A

esterifies free chol to FAs; derived from PTC in HDL memb; activ by ApoA; not endocytosed into liver whole like LDL; puts chol in, then goes around again

24
Q

CETP

A

glycoprot, transfers chol esters from HDL to LDL and VLDL and TAGs from LDL and VLDL to HDL; struc is long tunnel assoc w/HDL; genetic defect in this causes low heart disease; block this–>block chol transfer

25
Q

CETP inhibitors

A

Torcetrapib; raised HDL a lot, lowered LDL a lot, lowered TG a little; 60% inc in mortality; now Anacetrapib, w/o these effects

26
Q

ApoCIII

A

small proinflam prot, on surface of chylos, VLDL, LDL, HDL; most abund apolipoprot in humans; high levels –> atherosclerosis and <3 disease; exact fxn unknown

27
Q

HDL

A

high levels–>low inc of atherosclerosis; women have higher levels and less low levels and high inc of <3 dis

28
Q

lipoprot receptors

A

memb receps; med internalization of lipoprot particle, allow cells to acquire chol and other lipids

29
Q

LDLRs

A

7TM gene family; on PM of many cells (esp liver); bds to ApoB100 (on VLDL and LDL) and apo E (on chylos, VLDL, IDL); removes 70% of chol from circul; 839 AAs, 18 exons; 6 Cys that’re disulfide bonded; epidermal GF domain; oligosaccharide domain; transmemb; cyto domain

30
Q

scavenger receptors (SR)

A

bd to modified LDL (mLDL); also bd other anionic ligands; not subject to fdbk regulation like LDLR; on macs, dendritic cells, endothel cells

31
Q

LDLR epidermal GF homology domain

A

30%; 3 EGF repeats; 2 and 3 are sep by propeller region (sep LDL from receptor)

32
Q

cyto domain of LDLR

A

50 AAs; cont signal seq for internalization of receptor

33
Q

LDLR path and chol reg in liver

A

LDLRs are neg chg’d clustered in pits on memb; after bdg of LDL, whole complex endocytosed; LDLR sep fr LDL, recycled back to memb surface; LDL degraded by lysosomes, releasing free chol

34
Q

excess chol in liver reduced by

A

HMG CoA reductase syn., LDLR syn., HMG CoA reductase degrad (ubiquination), esterification (by ACAT-aCoA chol acyltransferase) and storage

35
Q

familial hypercholesterolemia

A

autosomal dominant; mutations in LDLR gene–>high chol levels (600-800mg/dl), premature absence/dysfxn of LDLR (1/2 in heteros); homos have xanthomas

36
Q

SR-A

A

on macs, endothel, sm m; recep for mLDL but not LDL; imp role in foam cell generation; no fdbk ctrl, so macs cont to accum chol (foam cells)

37
Q

SR-B

A

glycoprot w/509AA; large extracell loop w/2 TM domains; 8 Cys; on macs, adipocytes, liver; bd to LDL, mLDL, HDL; ApoA on HDL is ligand to this, plays role in transfer of chol fr HDL to liver cells

38
Q

SR-B deficiency

A

have high concs of chol, lg HDL particles

39
Q

atherosclerosis

A

16mln w/attack/stroke; fueled by inflam imm response

40
Q

intima

A

below endothel layer; mainly CT; in healthy, few scattered macs, SM cells, LDL; inflam process occurs here (chol accum, atherosclerosis occurs); LDL particles accum here (LDL transcytoses through endothel layer)

41
Q

mLDL

A

= OxLDL; macs, endothel, SM cells secrete inflam cytokines; LDL mod initiates atherosclerosis (foamy macs–>coalesce–>plaque)

42
Q

cap formation

A

atheroma is lipid pool w/foam cells, necrotic cells, free and esterified chol; cap forms on top w/macs, lymphocytes, and SMCs; SMCs sec collagen, elastin, proteoglycans to form fibrous matrix around cap

43
Q

proteases from macs

A

thin the cap at edges, causing rupture and contents come into contact w/procoag elements in blood–>acute thrombus occluding the lumen; areas exp to blood are platelet adhes sites, sec cytokines that perpetuate process, inc potential for thrombus/clot

44
Q

atheroma w/ or w/o plaque disruption

A

doesn’t nec completely occlude lumen; proc can be repeated mult times; only 20% lumen blocked when rupture takes place to completely block artery, on avg

45
Q

HDL removal of chol

A

chol can be remv’d from mac foam cells by transport via ACDA1 transporter to HDL (to liver for breakdown); req ApoA; reduces chol conc in plaques (sim to chol removal from periph cells by HDL)

46
Q

LDL driven atheroma resulting in stenosis

A

usu results in angina, can be detected by stress test/angiogram before attack

47
Q

LDL driven atheroma non-stentotic

A

not detected by angio/stress test; maj of plaque ruptures occur at areas w/o suff narrowing to be detected; worse b/c no pain, can’t detect until attack

48
Q

inc risk of inflam and athero

A

age, gender, smoking, obesity, T2DM, hypertension/ANG, menopause, high TAGs; other inflam dis like AD, psoriasis, asthma, arthritis, periodontal disease

49
Q

biochem markers for inflam detection

A

C-reactive prot; synth in liver; 5 monomers of 25000 MW each; adipocytes and macs synth IL6 cytokine, which induces liver to synth CRP; rise in inflam response somewhere (not specific to type of disease); elevated in cardiovasc disease; drop in ppl who exercise, stop smoking, lose weight; plaques less likely to rupture when CRP low; can have bad effect w/low LDL if high CRP

Biochem Unit 2 (13 decks)

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