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BCH MEtabolism > Lipids > Flashcards

Lipids Flashcards

1
Q

Types of lipids

A 
Fatty acids
Triacylglycerols
glycerolphospholipid
sphingolipids 
isoprene based lipids 
waxes
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2
Q

saturated

A

no double bonds

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3
Q

unsaturated

A

double bonds

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4
Q

palmitic acid

A

C16:0

get a present at sweet 16

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5
Q

stearic acid

A

C18:0

you get to steer a car at 18

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6
Q

oleic acid

A

C18:1

most abundant FA

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7
Q

Linoleic acid

A

C18:2

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8
Q

Arachidonic acid

A

C20:4

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9
Q

unsaturated fatty acids

A

double bonds are Cis form

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10
Q

Trans Fatty Acid

A

present at low levels in dairy and meat products

partially hydrogenated fats in foods contain much higher amts

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11
Q

Triacylglycerols/triglycerides

A

major source of energy
stored in adipose tissue
glycerol backbone
esterified to 3 fatty acids

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12
Q

Glycerolipids

A

glycerol back bone
fatty acids
ester linkage
phosphate - head groups

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13
Q

phospholipids

A

glycerol backbone (3C)
can have ether linkage
fatty acid - ester
phosphate - head groups

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14
Q

sphingolipids

A 
sphingosine backbone  (18C)
fatty acid 
amide linkage 
phosphate-head group
carbohydrate
ceramide= parent molecule
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15
Q

glycerophospholipds

A

saturated fatty acid C1
unsaturated fatty acid at C2
phosphate + head C3
phosphatidic acid= parent molecule

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16
Q

examples of glycerophospholipids

A 
phosphatidylcholine- lung surfactant
phosphatidylethanolamine- inner leaflet PM
phosphatidylserine-  inner leaflet PM
phosphatidylinositol- signaling 
cardiolipin - mitochondria
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17
Q

Ether glycerophospholipid

A

ether bond at C1
fatty acid C2
phosphate + head - C3

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18
Q

ether glycerophospholipid examples

A

plasmalogen
platelet activating factor - signaling , immune defense
short icicle chain at C2

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19
Q

sphingolipid examples

A

sphingomyelin - ceramide + choline head, structure
glycolipids- ceramid + sugars
cerebroside- 1 sugar
ganglioside- 3+ sugar

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20
Q

Steroids

A 
isoprene based molecule 
has three 6-membered rings 
one 5 membered ring 
all fused together 
functions as salt balance, metabolic, sexual function
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21
Q

Cholesterol

A

most common steroid

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22
Q

Lipid Biosynthesis

A 
intermediates in synthesis are linked to sulfylhydride groups of Acyl Carrier Proteins
Cytosol 
Fatty Acid Synthase 
NADPH, Malonyl CoA 
Insulin Induced
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23
Q

FormaFormation of Malonyl CoA activates

A

Acetate Units for Fatty acid synthase

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24
Q

Fatty acid Synthesis strategy

A

add of 2C units to growing chain
driven by decarboxylation of Malonyl CoA
elongation rxn repeated until growing chain is C16:0

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25
Q

Fatty Acid Synthesis regulators

A

high glucose
high ATP
low AMP
fatty acyl coA low

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26
Q

Sources for fatty acid synthesis

A

carbohydrates- mainly
fatty acids
amino acids

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27
Q

Rate limiting step

A

Acetyl CoA carboxylase

Acetyl CoA–> Malonyl CoA

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28
Q

Conversion of glucose to acetyl CoA for Fatty acid synthesis

A 
Glucose  enters liver
glycolysis
Pyruvate enters matrix
Pyruvate --> Citrate
Citrate leaves matrix 
Citrate --> OAA + Acety l CoA
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29
Q

pyruvate carboxylase

A 
pyruvate --> OAA  
acetyl coA (+)
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30
Q

pyruvate dehydrogenase

A 
pyruvate --> Acetyl CoA 
acetyl CoA (-)
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31
Q

citrate lyase

A

citrate –> OAA + acetyl CoA

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32
Q

fate of citrate –> OAA

A 
cytosolic malate dehydrogenase 
malic enzyme 
OAA--> malate--> pyruvate 
NADPH is produced 
uses ATP  
induced by insulin
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33
Q

Acetyl CoA supplies carbons for fatty acid synthesis using

A 
Acetyl CoA carboxylase 
Biotin 
CO2 
citrate (+) 
Rate limiting enzyme - target enzyme for lowering fat synthesis
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34
Q

what form is acetyl CoA carboxylase active?

A

nonphosphorylated

bc it is insulin regulated –> PPI

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35
Q

Fatty Acid Synthase

A

1 protein- 7 active sites - Vit B5 (pantothenic acid)

  1. Acyl Transferase- acetyl CoA primes the FA synthase
  2. Malonyl transfer - SH react with malonyl CoA
  3. Acetyl & Malonyl Condense
  4. Reduction, Hydration, Reduction
  5. Thioesterase- cleaves off FA
36
Q

where does Palmitate C16:0 undergo elongation and unsaturation

A

in the ER

37
Q

Elongation of FA requries

A

NADPH
Malonyl CoA
most prevalent form - Steric acid C18:0

38
Q

Unsaturation of FA

A

steraroyl-CoA desaturase
stearoyl-CoA (C18:0) –> Oleoyl-CoA (C18:1)
involves cytochrome b5 and cytochrome b5 reductase
NADH

39
Q

Arachidonic Acid synthesis

A

synthesized from linoleic acid (omega 6) C18:2

arachidonic acid C20:4

40
Q

essential fatty acids

A 
linoleic acid (diet) C18: 2 omega 6
linolenic acid (diet) C 18:3 omega 3
41
Q

EPA and DHA synthesis

A

from linolenic acid - omega 3

42
Q

Fatty Acid Breakdown

A 
intermediates in breakdown linked to SH groups of CoA 
occurs in mitochondria 
Beta oxidation
NADH, NAD+ 
glucagon induced
43
Q

What is the name of the process that oxidizes fatty acids to acetyl CoA?

A 
beta oxidation
oxidation 
hydration
oxidation 
thiolase
44
Q

where does beta oxidation occur?

A

mitochondrial matrix

45
Q

Entry of fatty acids is dependent on

A

fatty acid binding proteins

diffusion

46
Q

in circulation long chain fatty acids are bound to

A

albumin

47
Q

in cytosol, fatty acid binding proteins releases

A

fatty acid from albumin

and converts it to Fatty acyl CoA

48
Q

Transport of Long Chain FA requires

A

acyl CoA synthetase
Carnitine Palmitoyl transferase I (CPT I) on outer membrane
Translocase
CPT II on inner membrane

49
Q

Transport steps of FA

A
  1. FA crosses PM using fatty acid binding proteins
  2. fatty Acyl CoA diffuses outer membrane mito
  3. CPT 1 converts fatty acyl CoA to fatty acyl-carnitine
  4. fatty acyl-carnitine crosses inner membrane using translocate
  5. CPT II converts fatty acyl carnitine back to fatty acyl CoA
50
Q

Activation of Fatty Acids

A

formation of fatty acyl CoA - prereq to metabolism of Fatty acid in cell
Acyl CoA syntheses located in ER, outer mitochondrial membrane, peroxisomal membrane

51
Q

Fatty Acyl CoA fates

A

membrane lipids- ER
storage - TriacylGlycerols - ER
energy- Beta oxidation, ketogenesis - mitochondria

52
Q

Beta oxidation of LC FA enzymes

A
  1. Acyl CoA dehydrogenase
  2. hydrolase
  3. dehydrogenase
  4. thiolase
53
Q

Beta oxidation products

A

Fatty acyl CoA (C-2) –> B oxidation spiral

Acetyl CoA –> Krebs

54
Q

Beta oxidation vs Glucose oxidation

A

FA– 1 carbon: 8 ATP
Glucose – 1 C : 6.3 ATP

utilize glucose stores 1st - faster metabolism
then fats used for long term–
fats give off more energy but takes longer to metabolize

55
Q

oxidation of polyunsaturated fatty acid

A

cis bonds must be isomerize to Trans
reductase reduces conjugate bonds to 1 trans bond

Beta Oxidation relies on saturated FA

56
Q

oxidation of medium chain fatty acids

A

medium chain fatty acids = more water soluble than long chain
does not go through intestinal digestion – enter blood via hepatic portal vein
activated to CoA in liver
oxidized to Acetyl-CoA via B-oxidation

57
Q

oxidation of odd chain fatty acids

A

beta oxidation of odd carbon FA yields–> Propionyl CoA (3C)
propionyl- CoA–> –> —> Succinyl CoA
Biotin and B12

58
Q

Ketone bodies

A

special source of fuel and energy for certain tissues
source of fuel for brain, heart, muscle
major source for brain during starvation

59
Q

Where is ketone bodies made

A

produced in liver mitochondria matrix
but not used in the liver
can’t be broken down

60
Q

Ketone bodies reach target tissue mitochondria

A

converts back to acetoacetate and Beta hydroxybutyrate

61
Q

ketone body synthesis

A

acetyl CoA –> acetoacetyl CoA
HMG CoA sythase and lyase
Acetoacetate –> Beta-hydroxybutyrate + Acetone

62
Q

Synthesis of PC, PE, PS

A

Diacylglycerol –> phophatidylethanolamine / phosphatidylcholine
phosphatidylethanolamine –> phosphatidylcholine (use SAM)
Phosphatidylethanolamine –> phosphatidylserine

63
Q

Synthesis of Cardiolipin and phosphatidylinositol

A

Phosphatidic acid

—> Cardiolipin and Phosphatidyinositol

64
Q

Synthesis of Ether Glycerolipids

A
  1. DHAP + Fatty Acyl-CoA = Form Ester
  2. Fatty Acyl group exchanged for Fatty Alcohol= Fatty Acyl Alcohol
  3. Ether linkage is Formed
  4. Head group is added
65
Q

etholamine plasmalogen

A

found in myelin

synthesis occur in peroxisomes

66
Q

choline plasmalogen

A

found in heart muscles

synthesis occur peroxisomes

67
Q

Degradation of glycerolipids

A

phospholipase A1 cut at Carbon 1
Phospholipase A2 cut at Carbon 2
Phospholipase C cut at Carbon 3 releasing phosphate + head
Phospholipase D- cut at phosphate releasing head group

68
Q

phospholipases

A

in cell membranes or lysosomes
degraded based on needs of cell
tissue and organelle specific

69
Q

sphingolipid biosynthesis

A

Serine + palmitoyl-CoA
–> Ceramide (precursor for sphingolipids)
sphingolipids found in outer leaflet, PM, ER, Golgi

70
Q

Cholesterol Biosynthesis

A

occurs in Liver

  1. begins in cytosol
  2. uses 3 acetyl-CoAs
  3. HMG-CoA reductase (rate limiting step)
  4. Acetyl CoA–> maevalonate –> isoprene—>squalene
  5. squalene–> lanosterol (1st ring formed) –> cholesterol

uses ATP and NADPH

71
Q

Regulation of HMG-CoA reductase

A 
dephosphorylated = active (fed)
phosphorylated = inactive

half -life = 3 hrs
increase in cholesterol decreases gene expression for reductase

72
Q

Fates of cholesterol

A
    • bile salts
  • cholesterol esters (via Acyl-CoA cholesterol acyl transferase (ACAT)
  • hormones - progesterone, testosterone, cortisol, aldosterone
73
Q

Statins lower serum cholesterol levels by

A

targeting HMG CoA reductase

act as transition state analog

74
Q

how are lipids transported throughout the body

A

lipoproteins

75
Q

lipoproteins

A

cluster of lipids
monolayer membrane + apolipoprotein
polar surface = apolipoprotein, phospholipid, free cholesterol
nonpolar core- cholesteryl ester , TG, fats

76
Q

apoproteins

A

protein w/o lipid
has structural role
activate certain enzymes for lipoprotein metabolism
serve as ligands

77
Q

chylomicrons

A

apoB48, apo CII, apo E
apo CII activates Lipoprotein lipase (LPL) to release TG
remanants return to liver (driven by apoE receptors)

78
Q

VLDL

A 
apoB100 
HDL donates apoCII and apoE to form mature VLDL
LPL VLDL 
50 % remnants return to liver
50% remnants are in the form IDL
79
Q

IDL metabolism

A

HTGL removes core TG
forming LDL
60% return to liver via apoB100
40% carried to extra hepatic tissue

80
Q

LDL receptors

A

recognize apoB100 and apoE
binds all except for HDL
increasing cholesterol levels in cell inhibits LDL receptor synthesis
LDL receptor uptake= Endocytosis

81
Q

HDL synthesis

A

synthesis by liver and intestines

apoA1, apoAII, apoCI, apoCII

82
Q

Maturation of nascent HDL

A

accumulates phospholipids and cholesterol from cells lining the blood vessel
transfer of lipids to nascent HDL does nor require enzymatic activity
“brings cholesterol to liver” = good

83
Q

Reverse Cholesterol Transport

A

HDL remove cholesterol from ccells and return to liver
cells contain protein ABCA1 - use ATP hydrolysis to move cholesterol from inner to outer leaflet
HDL accepts cholesterol and modifies it
LCAT ensures cholesterol is linked to HDL

84
Q

Fate of HDL cholesterol

A

HDL can bind to receptors on hepatocytes
scavenger receptor SR-B1
not an endocytic mechanism

85
Q

HDL interacts with the lipoproteins

A

HDL converts nascent chylomicrons + VLDL –> mature form
CETP exchange pathway
transfer of cholesterol esters from HDL to VLDL in exchange for TG

86
Q

ATherosclerosis

A

inflammatory disease driven by oxidized LDL
macrophages express scavenger receptors that bind oxidized LDL
leads to foam cells in arterial walls (filled with lipids)
oxidized LDL cholesterol linked to coronary artery disease

BCH MEtabolism (8 decks)

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