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Unit 6 > Goody's Other Lectures > Flashcards

Goody's Other Lectures Flashcards

1
Q

Where does the NADPH needed for FA synthesis come from?

A

1) pentose-phosphate shunt

2) recycling of OAA (malate–>pyruvate–>citrate and NADPH)

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2
Q

What’s the rate-limiting step in fatty acid synthesis?

A

1) the first one!! (of course)
2) acetyl CoA–>malonyl CoA via ACC
3) requires ATP

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3
Q

Let’s talk about acetyl CoA carboxylase (ACC)

A

1) uses a biotin cofactor (needs ATP to attach CO2)**
2) needs citrate to polymerize (more active)
3) insulin dephosphorylates ACC and activates it
4) glucagon/epi phosphorylate ACC, turn it off
5) AMP/palmitoyl CoA feedback inhibit it

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4
Q

What are the steps of FA synthesis? (step 1 ACC, steps 2-5 catalyzed by fatty acid synthase (FAS))

A

1) activation
2) condensation formation of beta-keto group
3) reduction of beta-keto group
4) dehydrate a, b carbons
5) reduction of a, b bond
6) NADPH provides reducing equivalents

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5
Q

How does fatty acid synthase (FAS) work?

A

1) derived from B5 (pantothenic acid)
2) phospjo-pantetheinyl residue attached to acyl carrier protein part
3) SH group at bottom (sulfhydryl of phospho-pantetheinyl) reacts with malonyl CoA

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6
Q

How is palmitate made on FAS?

A

1) sequential malonyl CoA groups added, so 2 carbon groups added at a time
2) other steps in synthesis happen after, sequentially

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7
Q

What happens when palmitate leaves FAS?

A

1) palmitate activated to palmityl CoA
2) elongated by elongases
3) desaturation happens via desaturases (need O2, NADH, cytochrome B5)–this rxn only happens when carbs a plenty, in ER e- transport chain (uses an ER cytochrome b5)

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8
Q

What about MUFAs (monounsaturated fatty acids) and PUFAs (polyunsaturated fatty acids)?

A

1) delta 9 desaturase most active to create MUFAs

2) PUFAs omega-3 and omega-6 are essential since we can’t make them

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9
Q

What about arachidonic acid?

A

1) made by elongation and desaturation from linoleic acid

2) broken down into eicosanoids

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10
Q

What are eicosanoids?

A

1) signaling molecules, derived from arachidonic acid
2) include prostaglandins, thromboxanes, leukotrienes
3) involved in inflam response, smooth muscle constriction, bronchoconstriction or dilation
4) generated in situ, local mediators, unstable with short 1/2 life

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11
Q

What are the 3 pathways of eicosanoids and what do they form?

A

1) cyclooxygenase path: prostaglandins, thromboxanes, prostacyclins
2) lipoxygenase path: leukotrienes, lipoxins, hydroxyeicosatetraenoic acids (HETEs)
3) cytochrome P450 path: epoxides

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12
Q

Where do aspirin and other NSAIDs work?

A

1) they inhibit COX-1 and COX-2
2) stops conversion of arachidonic acid to PGH2
3) aspirin irreversibly inhibits, acetominophen/ibuprofen reversible

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13
Q

What is the rate-limiting step in the synthesis of steroid hormones from cholesterol?

A

1) cholesterol–>pregnenolone, catalyzed by cholesterol side-chain cleavage enzyme (goes from 30 carbons to 27 carbons)
2) enzyme located on the inner mitochondrial membrane
3) requires NADPH and O2

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14
Q

How do steroid hormones work at the molecular level?

A

1) diffuse through cytoplasm
2) bind a cytoplasmic or nuclear receptor once inside
3) ligand-receptor complex (bound to hormone) binds to hormone response element (HRE)
4) HRE is a specific regulatory sequence in promotor or enhancer element, hormone-specific
5) binding of HRE and complex causes conformational change, complex can interact with DNA and transcription can begin!

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15
Q

What happens to steroid hormones?

A

1) inactivated and conjugated in liver

2) now water soluble, they can be kicked out in bile, pee, or poop

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16
Q

What’s the active form of vitamin D?

A

1) 1,25-dihydroxycholecalciferol (1, 25-diOH-D3, calcitriol)

2) it’s a sterol (all D vitamins are) that acts like a steroid hormone (monitors transcription)

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17
Q

What’s the endogenous source of vitamin D?

A

1) sunlight hits epidermis/dermis
2) 7-dehydrocholesterol–>cholecalficerol
3) cholecalciferol transported to liver

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18
Q

What’s the exogenous source of vitamin D?

A

1) ergocalciferol (vitamin D2)
2) cholecalciferol (vitamin D3)
3) dietary vitamin D packed into chylomicrons

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19
Q

How is inactive vitamin D converted to active vitamin D?

A

1) cholecalciferol–>25-hydroxycholecalciferol (calcidiol), via 25 hydroxylase (rxn in liver)
2) calcidiol–>calcitriol via 25-hydroxycholecalciferol 1-hydroxylase (rxn in kidney)
3) both hydroxylases are cytochrome P450s

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20
Q

What triggers 25-hydroxycholecalciferol 1-hydroxylase activity?

A

1) directly increased by low plasma phosphate
2) indirectly increased by low plasma calcium (causes PTH stimulation and subsequent upregulation of enzyme)
3) elevated calcitriol inhibits enzyme (feedback)

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21
Q

How does vitamin D help in intestinal Ca+2 absorption?

A

1) enters cell, binds to vitamin D receptor
2) complex moves to nucleus, activates certain areas
3) calbindin upregulated, aids Ca+2 in entering enterocyte

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22
Q

What are the glycerophospholipids?

A

1) phosphatidylcholine
2) phosphatidylserine
3) phosphatidylethanolamine
4) PIP2
5) phosphatidyglycerol
6) cardiolipin
7) glycerol backbone, 2 fatty acid chains, phosphate/head group

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23
Q

What are the ether glycolipids?

A

1) plasmalogens
2) platelet activating factor (PAF)
3) glycero-ether backbone/side chain, FA side chain, phosphate/head group

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24
Q

What are the sphingolipids?

A

1) sphingophospholipids (sphingomyelin)
2) glycolipids (cerebrosides, sulfatides, globosides, gangliosides)
3) sphingomyelin has sphingosine backbone, an FA chain, a phosphate/head group
4) glycolipids have sphingosine/FA-like backbone, a FA, and a carbohydrate

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25
Q

Describe the backbone of sphingomyelin

A

1) sphingosine backbone is an amino alcohol
2) the additional attached FA makes the sphingosine a ceramide (sphingosine/FA are ceramide by definition)
3) choline is attached to the phosphate

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26
Q

Describe the glycoplipids

A

1) galactocerebroside and glucocerebroside are cerebrosides (a ceramide and a sugar group, monosaccharide)
2) globosides are ceramide oligosaccharides (ceramide and multiple sugars attached)
3) gangliosides are glycosphingolipids, globoside derivatives (ceramide+oligosaccharide with 1 or more sialic acid derivatives), have neg charge

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27
Q

What’s the distribution of complex lipids in the cell membrane and how do they move about?

A

1) choline-containing face external surface (sphingomyelin, glycolipids, phosphatidylcholine)
2) amine-containing face cytosol (phosphatidylserine, phosphatidylethanolamine, phosphatidylinositol)
3) scramblases/floppases flip PL/SM down concentration gradient (don’t require ATP)
4) flippases flip PL/SM against concentration gradient (require ATP)

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28
Q

How are glycerophospholipids synthesized?

A

1) 2 activated fatty acyl chains+glycerol–>phosphatidic acid (PA)
2) phosphatidic acid–>DAG + CDP-head group–>gylcerophospholipid–>PC, PE, PS
3) phosphatidic acid–>CDP-DAG + head-group–>glycerophospholipid–>PI, cardiolipin, PG
4) interconverions between phospholipids can happen (PS–>PE, PE–>PS, PE–>PC, etc.)

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29
Q

What’s lung surfactant and why is it important?

A

1) dipalmitoylphosphatidylcholine (DPPC) is PC w/C1 and C2 esterified to palmitate
2) deficiency in its synthesis in lungs causes increased surface tension, alveolar collapse, and respiratory distress

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30
Q

How are cardiolipin and PI (phosphatidylinositol) made?

A

1) phosphatidic acid–>CDP-DAG + phosphatidylglycerol–>cardiolipin
2) phosphatidic acid–>CDP-DAG + inositiol–> PI+kinase–>phsophatidylinositol bisphosphate (PIP2)

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31
Q

How is plasmalogen made?

A

1) DHAP–>ethanolamine plasmalogen

2) rxns take place in peroxisomes; problem in people with Zellweger syndrome (decrease in # functional peroxisomes)

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32
Q

How is ceramide made?

A

1) serine+palmitoyl CoA–>dihydrosphingosine+fatty acyl group–>ceramine

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33
Q

Where are sphingolipids made?

A

in the Golgi

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34
Q

How is sphingomyelin made?

A

1) ceramide + phosphatidylcholine –>sphingomyelin

2) DAG is lost in rxn

35
Q

How are galactocerebrosides and sulfatides made?

A

1) ceramide+UDP-galactose–>galactocerebroside

2) galactocerebroside–>sulfatide, charged (rxn needs PAPS, a sulfotransferase)

36
Q

How are glucocerebrosides, gangliosides, and globosides made?

A

1) ceramide+UDP-glucose–>glucocerebroside
2) glucocerebroside+UDP-sugars+CMP-NANA–>ganglioside
3) glucocerebroside+extra sugars–>globoside (extra sugars added by glycosyl transferases)

37
Q

What do the phospholipases A1/A2 do?

A

1) they can remove FA chains from membrane-associated phospholipids (can aid in phospholipid remodeling)
2) they cleave off FA at C1/C2, leaving behing lysophospholipids
3) phospholipase A2 can release arachidonic acid

38
Q

What does phospholipase D do?

A

1) cleaves off the head group of phospholipid, leaving behind phosphatidic acid (PA)

39
Q

What does phospholipase C do? How is it activated?

A

1) cleaves off the phosphorylated head group yielding DAG
2) GPCR activation causes it to cleave PIP2, yielding DAG and IP3
3) DAG causes increase in Ca+2
4) IP3 causes activation of protein kinase C

40
Q

How is cholesterol made and what happens to it?

A

1) enters via diet or made mainly by liver; can be made by all cells (except RBCs)
2) leaves liver as unmodified free cholesterol (in bile)
3) is converted to bile acids/salts in liver, enters GI lumen
4) joins VLDL and sent into blood from liver

41
Q

Describe the structure of cholesterol

A

1) 4 planar HC rings, called steroid nucleus, and an HC tail, alcohol group at C3 (amphiphilic), molecule is a sterol isoprenoid
2) most cholesterol in blood is esterified to a FA acid C3; this version even more hydrophobic than actual cholesterol
3) in membrane, increases strength and decreases fluidity

42
Q

What does ezetimibe do?

A

1) blocks cholesterol intestinal absorption at enterocyte brush border

43
Q

Describe the first steps of cholesterol synthesis

A

1) rxns occur on cytoplasmic surface of smooth ER, need ER membrane/cystosolic enzymes
2) 2 acetyl CoA–>acetoacetyl CoA (via thiolase)
3) acetoacetyl CoA–>HMG CoA (via cytosolic HMG-CoA synthase)
4) HMG-CoA–>mevalonate (via HMG-CoA reductase, integral smoot ER membrane protein), rxn requires 2 molecules of NADPH, CoA released so rxn irreversible

44
Q

What are the next steps of cholesterol synthesis?

A

1) mevalonate+2ATP–>6 C + ATP–> IPP (5C isoprene)–>DPP (5C isomer)
2) IPP+DPP–>GPP (10 C)+IPP–>FPP (15 C)
3) FPP+FPP–>squalene, 30 C, has 6 isoprenoid units (pyrophosphate released, molecule reduced)
4) since 3 ATP for every mevalonate, 18 ATP needed to make polyiosprenoid squalene

45
Q

How does squalene become cholesterol?

A

1) squalene–>lanosterol+NADPH+O2–>cholesterol
2) all products in this path are hydrophobic, need a sterol carrier protein so they’re soluble in cytoplasm
3) Smith-Lemli-Opitz syndrome is a genetic deficiency of the enzyme that reduces the last double bond and makes cholesterol

46
Q

How is cholesterol synthesis regulated?

A

1) SREBP-2 (sterol regulatory element binding protein 2) binds SRE (sterol regulatory element)
2) SREBP-2 associates with SCAP (SREBP cleavage-activating protein, ER protein)
3) SREBP-2-SCAP moves to Golgi when cholesterol is low, stimulates cleavage/activation of SREBP as a transcr factor
4) SREBP goes to nucleus, binds SRE, stimulates expression of HMG-CoA reductase
5) when cholesterol high, it binds to sterol domain of SCAP, so SREBP-2-SCAP can’t leave ER membrane; cholesterol synthesis decreases
6) when cholesterol high, it also binds to sterol domain of HMG CoA reductase itself, triggers ubiquitination/degradation of enzyme
7) AMP-activated protein kinase and phosphoprotein phosphatase phosphorylate enzyme (inactivate it) when ATP low and AMP high
8) insulin/thyroxine upregulate expression of HMG CoA reductase gene, glucagon/glucocorticoids downregulate expression

47
Q

How do statin drugs work?

A

1) structural analogs of HMG
2) are competitive inhibitors of HMG CoA reductase
3) lower blood cholesterol levels

48
Q

Give a general description of bile/bile acid synthesis

A

1) bile is a mixture of bile salts, phosphatidyl choline, organic/inorganic molecules
2) the carboxyl groups have a pKa of 6, which is the duodenal pH, so in lumen 1/2 protonated (bile acids) and 1/2 deprotonated (bile salts)
3) bile acids/salts have a polar and nonpolar face, aids in emulsification
4) rate-limiting step is addition of hydroxyl group at C7 of cholesterol, makes it 7-alpha-hydroxycholesterol (catalyzed by cholesterol-7-alpha-hydroxylase, enzyme expression down regulated by bile acids)

49
Q

How are bile salts conjugated?

A

1) in liver, become either serine or taurine; they have lover pKa and are fully ionized at alkaline pH of bile
2) only conjugated forms of bile salts are found in bile

50
Q

What happens to the bile salts?

A

1) bacteria can unconjugate conjugated bile salts

2) albumin binds and transports bile salts in blood, returns them to liver

51
Q

Describe cholelithiasis

A

1) cholesterol moving into bile has to occur with mvmt of bile salt and phospholipid secretion
2) if dual secretion process messed up (not enough bile salt production or increased cholesterol), imbalance occurs and cholesterol can’t be solubilized enough by bile salts and phospholipids
3) causes precipitation of cholesterol forming gallstones
4) Sx is laproscopic cholecysectomy

52
Q

Describe plasma lipoproteins

A

1) spherical complexes of lipids/specific proteins called apolipoproteins
2) chylomicrons, VLDL, IDL, LDL, HDL are all lipoproteins
3) they protect hydrophobic cargo, allow it to move in blood as it goes from one tissue to another

53
Q

What’s the general lipoprotein structure?

A

1) inner hydrophobic core full of TG/cholesterol esters (hydrophobic)
2) apolipoproteins, unesterified cholesterol, phospholipids face outside (hydrophilic)

54
Q

What does A-I do?

A

1) most abundant apo-LP in HDL
2) made by liver and intestine
3) activates LCAT (lecithin-cholesterol acyl transferase), which converts free cholesterol into cholesterol ester–this action helps “mature” HDL (whatever that means)
4) considered antiatherogenic protein

55
Q

What does A-II do?

A

1) made by liver
2) found w/AI in HDL
3) activates LPL and inhibits LCAT–therefore, may be proatherogenic

56
Q

What does ApoB-100 do?

A

1) made by liver
2) structural VLDL protein, helps VLDL assemble (one per each VLDL, stays with it as it goes to IDL/LDL)
3) higher apoB levels means CVD

57
Q

What does apoB-48 do?

A

1) made by gut, structurally 48% of apoB100
2) involved in chylomicron (CM) metabolism
3) not recognized by LDLR

58
Q

What do the ApoCI/II/III do?

A

1) can be exchanged between LP particles
2) can either interfere with apoE recognition by LP receptors or displace apoE from LP
3) apoCII activates LPL (lipoprotein lipase)
4) apoCIII inhibits LPL
5) made by liver

59
Q

What do the apoEs do? (E2, E3, E4)

A

1) made by liver
2) associated with all LPs except LDL
3) recognized by LDLR and LRP (LDL receptor-related protein), helps liver take up CM/VLDL/IDL
4) responsible for clearing the gut of intestinal LPs after eating and clearing VLDL/IDL before they become LDL

60
Q

Describe CM (chylomicron) metabolism

A

1) when chylomicron gets to blood, apo-E attaches (for hepatic recognition) and apo-Cs from HDL particles join
2) LPL activated by apoCII, hydrolyzes CM
3) fatty acids stored or used as energy, glycerol goes back to liver
4) LPL activity cases CM to get smaller and more dense
5) apo-Cs returned to HDL, what’s left over is called chylomicron remnant
6) apo-E on CM remnant allows liver to take it up; receptors recycled, degraded into cholesterol/amino acids/fatty acids

61
Q

What happens with a deficiency of LPL?

A

1) chylomicron TAG accumulate in plasma, since chylomicrons can’t be broken down
2) higher risk for pancreatitis
3) called type 1 hyperlipoproteinemia, familial LPL deficiency

62
Q

How is VLDL metabolized?

A

1) VLDL made in liver, their role is to carry lipids from liver to peripheral tissues (body’s main transporter for CE/TG/PL/cholesterol esters)
2) TGs transferred from VLDL to HDL, cholesterol transferred from HDL to VLDL via cholesterol ester exchange protein (CETP)
3) TGs degraded by LPL (same as in CMs)–>IDL (lose apoE receptors)–>when cholesterol more than TG, IDL–>LDL

63
Q

How does CETP (cholesterol ester transfer protein) work?

A

1) moves TG from VLDL–>HDL
2) moves cholesterol ester from HDL–>VLDL
3) the more TG-containing LPs in blood, the faster this exchange happens–meaning lots of TG-containing LPs causes more cholesterol to get to liver via VLDL/IDL

64
Q

What happens to LDL?

A

1) LDL has a lot less TG than VLDL, but it has more cholesterol and cholesterol esters–this is the BAD cholesterol
2) they bring cholesterol to periphery
3) LDL receptors bind LDL, LDL endocytosed via clathrin-coated pits (recognition of apo-B100 and apoE)
4) LDL contents released by lysosomes, receptors recycled to membrane
5) people with LDL-receptor deficiency have type II hyperlipidemia (FH, familial hypercholesterolemia)
6) oversupply of cholesterol can stop expression of liver LDL receptor

65
Q

What happens to HDL?

A

1) they supply apoCII and apoE in circulation
2) take up cholesterol from periphery and return it to liver as cholesterol esters (liver uses it for bile synthesis); also delivers cholesterol to steroidogenic cells to make hormones–GOOD cholesterol
3) apoA-I activates LCAT, which esterifies cholesterol; it maintains the concentration gradient so HDL can continue to pick up cholesterol
4) CETP takes cholesterol from HDL and gives it to VLDL, it takes TG from VLDL and gives them to HDL

66
Q

How do plaques form?

A

1) oxidized/damaged LDL causes endothelial injury, so macrophages come and digest damaged LDL
2) macrophages become foam cells
3) foam cells accumulate, releasing growth factors/cytokines–>inflamm rxn
4) plaque forms within the BV, a cap forms over the “roof” which extends into the lumen and partially occludes it
5) smooth muscle from media thins the fibrous cap; cap eventually ruptures
6) procoags in circulation bind, inflamm/thrombus formation
7) if thrombus eventually completely occludes the lumen, MI can happen

67
Q

What does LDL-R do?

A

1) major recognition protein for apoB100 and apoE

2) involved in LDL uptake; deficiency causes FH

68
Q

What does LDLR-related protein do?

A

1) recognizes ApoE, not apoB100
2) helps mediate reuptake of CM remnants and VLDL
3) helps in metabolism of apoE containing LPs, but not LDL metabolism

69
Q

What does scavenger receptor A do?

A

1) helps uptake oxidized LDL into macrophages

2) this helps create foam cells (bad)

70
Q

What does scavenger receptor B do?

A

1) CD36/SR-B1

2) helps uptake cholesterol from HDL by the liver and steroid-hormone making tissues

71
Q

What does apoB-48 do?

A

1) made by gut, structurally 48% of apoB100
2) involved in chylomicron (CM) metabolism
3) not recognized by LDLR

72
Q

What do the ApoCI/II/III do?

A

1) can be exchanged between LP particles
2) can either interfere with apoE recognition by LP receptors or displace apoE from LP
3) apoCII activates LPL (lipoprotein lipase)
4) apoCIII inhibits LPL
5) made by liver

73
Q

What do the apoEs do? (E2, E3, E4)

A

1) made by liver
2) associated with all LPs except LDL
3) recognized by LDLR and LRP (LDL receptor-related protein), helps liver take up CM/VLDL/IDL
4) responsible for clearing the gut of intestinal LPs after eating and clearing VLDL/IDL before they become LDL

74
Q

Describe CM (chylomicron) metabolism

A

1) when chylomicron gets to blood, apo-E attaches (for hepatic recognition) and apo-Csfrom HDL particles joins
2) LPL activated by apoCII, hydrolyzes CM
3) fatty acids stored or used as energy, glycerol goes back to liver
4) LPL activity cases CM to get smaller and more dense
5) apo-Cs returned to HDL, what’s left over is called chylomicron remnant
6) apo-E on CM remnant allows liver to take it up; receptors recycled, degraded into cholesterol/amino acids/fatty acids

75
Q

What happens with a deficiency of LPL?

A

1) chylomicron TAG accumulate in plasma, since chylomicrons can’t be broken down
2) higher risk for pancreatitis
3) called type 1 hyperlipoproteinemia, familial LPL deficiency

76
Q

How is VLDL metabolized?

A

1) VLDL made in liver, their role is to carry lipids from liver to peripheral tissues (body’s main transporter for CE/TG/PL/cholesterol esters)
2) TGs transferred from VLDL to HDL, cholesterol transferred from HDL to VLDL via cholesterol ester exchange protein (CETP)
3) TGs degraded by LPL (same as in CMs)–>IDL (lose apoE receptors)–>when cholesterol more than TG, IDL–>LDL

77
Q

How does CETP (cholesterol ester transfer protein) work?

A

1) moves TG from VLDL–>HDL
2) moves cholesterol ester from HDL–>VLDL
3) the more TG-containing LPs in blood, the faster this exchange happens–meaning lots of TG-containing LPs causes more cholesterol to get to liver via VLDL/IDL

78
Q

What happens to LDL?

A

1) LDL has a lot less TG than VLDL, but it has more cholesterol and cholesterol esters–this is the BAD cholesterol
2) they bring cholesterol to periphery
3) LDL receptors bind LDL, LDL endocytosed via clathrin-coated pits (recognition of apo-B100 and apoE)
4) LDL contents released by lysosomes, receptors recycled to membrane
5) people with LDL-receptor deficiency have type II hyperlipidemia (FH, familial hypercholesterolemia)
6) oversupply of cholesterol can stop expression of liver LDL receptor

79
Q

What happens to HDL?

A

1) they supply apoCII and apoE in circulation
2) take up cholesterol from periphery and return it to liver as cholesterol esters (liver uses it for bile synthesis); also delivers cholesterol to steroidogenic cells to make hormones–GOOD cholesterol
3) apoA-I activates LCAT, which esterifies cholesterol; it maintains the concentration gradient so HDL can continue to pick up cholesterol
4) CETP takes cholesterol from HDL and gives it to VLDL, it takes TG from VLDL and gives them to HDL

80
Q

How do plaques form?

A

1) oxidized/damaged LDL causes endothelial injury, so macrophages come and digest damaged LDL
2) macrophages become foam cells
3) foam cells accumulate, releasing growth factors/cytokines–>inflamm rxn
4) plaque forms within the BV, a cap forms over the “roof” which extends into the lumen and partially occludes it
5) smooth muscle from media thins the fibrous cap; cap eventually ruptures
6) procoags in circulation bind, inflamm/thrombus formation
7) if thrombus eventually completely occludes the lumen, MI can happen

81
Q

What does LDL-R do?

A

1) major recognition protein for apoB100 and apoE

2) involved in LDL uptake; deficiency causes FH

82
Q

What does LDLR-related protein do?

A

1) recognizes ApoE, not apoB100
2) helps mediate reuptake of CM remnants and VLDL
3) helps in metabolism of apoE containing LPs, but not LDL metabolism

83
Q

What does scavenger receptor A do?

A

1) helps uptake oxidized LDL into macrophages

2) this helps create foam cells (bad)

84
Q

What does scavenger receptor B do?

A

1) CD36/SR-B1

2) helps uptake cholesterol from HDL by the liver and steroid-hormone making tissues

Unit 6 (8 decks)

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