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Biochemistry > FAs, Lipids, and Cholesterol > Flashcards

FAs, Lipids, and Cholesterol Flashcards

1
Q

End Point of FA Synthesis

A

Palmitic Acid

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2
Q

Getting Acetyl CoA into Cytosol for FA Synthesis (3 Steps)

A

ATP binds isocitrate dehydrogenase and inhibits it, causing buildup of citrate
Citrate moved out of mt matrix into cytosol
ATP-citrate lyase acts as opposite of citrate synthase and cleaves it into OAA and Acetyl CoA

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3
Q

Acetyl CoA Carboxylase (2)

A

Gateway to FA synthesis

Converts Acetyl CoA to Malonyl CoA via carboxylation

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4
Q

Acetyl CoA Carboxylase Regulation

A

AMP-dependent kinase (AMPK) phosphodeactivates it into inactive dimer under starving/epinephrine conditions, whereas protein phosphatase dephosphoactivates it into active polymer from insulin

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5
Q

Process of FA Synth (7)

A

Acetyl CoA attaches to cysteine residue of carrier prot
Malonyl CoA attaches to modified pantothenate on that prot
Malonyl decarbox’d, new carbanion attacks acetyl group
Reduction of last carbonyl group via NADPH
Dehydration of new OH/H
Reduction of new double bond via NADPH
Transfers to cysteine residue, new malonyl CoA added to pantothenate, cycled continues to palmitate (16C)

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6
Q

NADPH Production Associated w/ FA Synthesis (2 steps)

A

Cytosolic NADH-dependent malate dehydrogenase converts OAA to malate. NADP+ dependent malate dehydrogenase converts malate to pyruvate and creates NADPH from it

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7
Q

2 Sources of Glycerol PO4 production in Liver

A

Dihydroxyacetone P from glycolysis converted via glycerol-P dehydrogenase
Glycerol converted via Glycerol kinase

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8
Q

1 Source of Glycerol P Production in Adipose Tissue

A

DHAP from glycolysis converted via glycerol-P dehydrogenase

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9
Q

TAG Synthesis (3)

A

Acyltransferases add to glycerol P twice until its phosphatidic acid
Phosphatase then removes PO4 so its diacylglycerol (DAG)
Acyltransferase then adds acyl so its triacylglycerol (TAG)

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10
Q

Hormone-Sensitive Lipase

A

Activated by protein kinase from glucagon/epinephrine, breaks down TAGs

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11
Q

Carnitine Shuttle (purpose and mech[2])

A

To transport LC FA-CoA from cyt to mt matrix without risk of synthesized FAs going right back in to matrix
Fatty acyl CoA transported to IM space, where carnitine palmitoyl-transferase I switches CoA for Carnitine
Then Fatty Acyl Carnitine transported to matrix, where carnitine palmitoyl transferase II switches back to Fatty Acyl CoA

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12
Q

Beta Oxidation Rxns (4)

A

Oxidation of C2/3 yields double bond and produces FADH2
Hydration of double bond at C3
Oxidation of C3 hydroxyl, yielding NADH
Thiolysis w/ addition of CoA creating Acetyl CoA and Fatty acyl CoA (2Cs shorter)

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13
Q

3 Products from Full Beta Oxidation of Palmitoyl CoA

A

7 FADH2, 7 NADH, and 8 Acetyl CoA

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14
Q

Beta Oxidation of Odd-Number Chain FAs

A

Go through separate pathway where coenzyme form of Vit B12 eventually converts Methylmalonyl-CoA to Succinyl CoA for TCA cycle

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15
Q

Ketone Body Synthesis (4)

A

FA Beta Oxidation yields Acetoacetyl CoA
HMG CoA Synthase adds another acetyl CoA to form HMG CoA
HMG CoA lyase removes acetyl CoA to form acetoacetate
3-Hydroxybutyrate dehydrogenase converts to 3-Hydroxybutarate

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16
Q

Phospholipid Synthesis

A

CTP activates phosphatidic acid by adding CDP to diacylglycerol, and then an alcohol w/ head group can add

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17
Q

Cleaving Points for the 4 Phospholipases

A

A1: C1 acyl group
A2: C2 acyl group
C: C3 after the O, before the P
D: C3 polar head group but leaves the P

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18
Q

Phospholipase C Important Mech Involvement

A

Cleaves Phosphatidyl-inositol 4,5-bisphosphate to IP3 and DAG

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19
Q

Niemann-Pick Disease (3)

A

Sphingomyelinase deficiency (sphingolipidosis)
Causes buildup of sphingomyelin and prevents ceramide release
Foamy appearing cells containing sphingomyelin under microscope

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20
Q

Cerebroside

A

Ceramide w/ sugar residue

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21
Q

Ganglioside

A

Cerebroside w/ charged COO- on terminal sugar

22
Q

Sulfatide

A

Cerebroside w/ OSO3- on terminal sugar

23
Q

Tay-Sachs Disease (4)

A

Sphingolipidosis
Beta-Hexosaminidase A deficiency
Causes accumulation of gangliosides (specifically NANA)
Prevents ceramide release

24
Q

Gaucher Disease (4)

A

Sphingolipidosis
Beta-glucosidase deficiency
Causes buildup of glucocerebrosides
Prevents ceramide release

25
Q

Prostaglandin Synthesis (4)

A

Dietary linoleic acid converted into arachidonic acid, which COX converts to PGG2 w/ 2 O2, and then peroxidase converts into PGH2, which differentiates into the different prostaglandins

26
Q

2 Fates of Arachidonic Acid

A

5-Lipoxygenase converts to Leukotrienes

COX-1 or 2 modify to PGG2

27
Q

2 Prostaglandins and Function

A 
Thromboxane A2 (TXA2) promotes platelet aggregation
Prostacyclin (PGI2) in endothelium of blood vessels, promoting vasodilation
28
Q

Aspirin Mech (3)

A

Acetylates serine side chain in COX active site, preventing prostaglandin synthesis
Platelets don’t have nuc, so TXA2 inhibition means they’re done so blood thinning
Endothelial cells can just degrade COX and make more, so PGI2 still fine

29
Q

Rate-Limiting “Gateway” into Cholesterol Biosynthesis

A

HMG CoA reductase converts HMG CoA to mevalonate

30
Q

Synthesis of Cholesterol Mevalonate->on (7)

A

6C mevalonate phopho’d twice to form 5-pyrophosphomevalonate
Decarbox’d to isopentenyl pyrophosphate (IPP) (5C)
Isomerized to dimethylallyl pyrophosphate (DPP) (5C)
IPP added to form Geranyl pyrophosphate (10C)
IPP added to form farnesyl pyrophosphate (15C)
2 of those form Squalene (30C)
Then hydroxy added and other modifications to turn it into cholesterol

31
Q

Stimulation of HMG CoA Reductase Activity (2)

A

Phosphoprotein phosphatase dephosphoactivates it

SREBP also binds SRE, stimulating transcription of HMG CoA Reductase

32
Q

Inhibition of HMG CoA Reductase (2)

A

AMPK phosphodeactivates

Cholesterol inhibits SREBP release from Golgi

33
Q

Statins Action

A

Lower cholesterol my inhibiting HMG CoA Reductase

34
Q

Bile Acid Synthesis

A

Cholesterol 7-alpha-hydroxylase adds carboxylic acid to cholesterol alkane tail to for cholic acid or chenodeoxycholic acid

35
Q

Bile Salt Synthesis (2)

A

Glycine added to cholic acid to make glycocholic acid

Taurine added to chenodeoxycholic acid to make Taurochenodeoxycholic acid

36
Q

Enterohepatic Circulation

A

Bile salts/acids sent from liver/gallbladder to intestines and those that aren’t excreted are recycled back to liver

37
Q

Steroid Synthesis (7 different molecules mentioned total)

A

Cholesterol to pregnenolone to progesterone which differentiates into cortisol, aldosterone, or testosterone (and then estradiol from there)

38
Q

Congenital Adrenal Hyperplasias (CAH)

A

Deficiencies in enzymes along the steroid hormone synthesis pathway

39
Q

General Passage of Cholesterol Through Lipoproteins (5)

A

Chylomicrons w/ lots of TAGs go from GI to muscles/tissues
Remnants go to liver
Contents repackaged into VLDL w/ some TAGs and cholesterol which goes to tissues
LDL returns to liver w/ just cholesterol and cholesteryl esters
HDL then secreted in bile, takes up cholesterol from peripheral tissues and returns

40
Q

Lipoprotein w/ Highest TAG component

A

Chylomicrons

41
Q

Lipoprotein w/ Highest Cholesterol Component

A

LDL

42
Q

Chylomicron Apolipoproteins (3 prots, 5 points)

A

Apo B-48 added upon nascent in SI
Then C-II and Apo E added from HDL
C-II activates lipoprotein lipase to hydrolyze TAGs to FAs and glycerol in capillaries
Then Apo C-II returned to HDL from remnant
Apo E binds to Rs in liver for endocytosis of the remnant

43
Q

VLDL and LDL Apolipoproteins (3 prots, 5 points)

A

Apo B-100 on nascent VLDL in liver
Then Apo C-II and Apo E added from HDL
Apo C-II activates lipoprotein lipase to hydrolyze TAGs to FAs and glycerol in capillaries
Apo C-II and Apo E returned to HDL from LDL (which now has CEs and C almost entirely)
Apo B-100 binds to LDL Rs on extrahepatic/liver tissues and are endocytosed

44
Q

Cholesteryl Ester Transfer Protein (CETP)

A

Catalyzes transfer of TAGs to HDL from VLDL and CE from HDL to VLDL

45
Q

Difference b/w Apo B-100 and Apo B-48

A

Come off same gene w/ same mRNA, but a cytosine is edited in ssRNA to create a stop codon to make Apo B-48 for chylomicrons

46
Q

Familial Hypercholesterolemia

A

Low LDL Rs causes hypercholesterolemia

47
Q

PCSK9

A

Gene for LDL R degrading protein on outside of the cell, new even more effective target for inhibition decreasing cholesterol

48
Q

2 Inhibitory Effects by Cholesterol

A

Blocks HMG CoA Reductase

Blocks synthesis of LDL Rs

49
Q

Cholesterol’s Contribution to Arterosclerosis (major point and 4 steps)

A

Individual has to have high cholesterol AND unknown susceptibility to oxidative
Endothelium causes/releases oxidative stress
LDLs damaged by it
Macrophages swallow damaged LDLs and become foam cells
Foam cells deposit onto arterial walls causing plaques

50
Q

HDL Circulation

A

Released as bile and then has intermediate stages which pick up cholesterol from peripheral tissues and return to liver

Biochemistry (23 decks)

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