Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Nutrition And Metabolism > Lipids > Flashcards

Lipids Flashcards

1
Q

Lipids classification

A

Fatty acids
Vit fat soluble ( A,E,K,D)
Phospholipids

Amphipatics :

Sphingolipids
Triacylglycerol
Glycolipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Triacylglycerol structure

A

3 fatty acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Types of triacylglycerol in natural oils

A

Unsaturated FAs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Primary target of salivary lipase

A

Fewer than 12C tTAGs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Solid fats composed mostly of

A

Saturated fats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Calories of fat per gram

A

9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Functions of fats

A 
Structure of cells 
Enzyme cofactor 
Vision 
Digestion 
Anti oxidant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Daily fat consumption average

A

60-160g

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Thé 2 essential dietary fatty acid

A

Linoleic acid which gives arachidonic acid

a-linolenic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Bile acid production rate limiting step

A

Cholic acid synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Bile acid synthesis pathway

A

Cholesterol to cholic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Bile salts formation location

A

Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pancreatic lipase action on TGs

A

Break it down to 2-monoacylglycerol

And free fatty acids at carbon 1 and 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When is stored fat used ?

A

When there’s non availability or inadequacy of carbohydrates or the impossibility of metabolizing them for energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What hormone ca activate lipase?

A

Glucagon
Epinephrine
Nor epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How can insulin inhibits lipase activity

A

Insulin promotes dephosphorylation of lipase by cAMP and PKA inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Acetyl coa carboxylase in fatty acid synthesis is inhibited by …

A

Hormone mediated phosphorylation so cAMP activation inhibits it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Rate limiting step in fatty acids synthesis

A

Acetyl coa carboxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How are fatty acids transported into blood

A

Serum albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Fate of glycerol produced by TGs degradation

A

Goes to liver

Converted to dihydroxyacetone phosphate by glycerol kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Fate of fatty acids after activation

A

Can be broken down to form CO2

Can be used to produce TGs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Activation of fatty acids done by

A

Acyl coa synthétase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where does fatty acid activation occur

A

Outer mitochondrial membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Product of fatty acid activation

A

Acyl Coa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Transport of acyl coa into mitonchondria ( less than 12c)

A

Passive diffusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Transport of acyl coa into mitonchondria ( more than 12c)

A

Acyl coa converted to acyl carnitine and converted back to acyl coa once inside

Done by carnitine acyltransferase I (outer) and II (inner)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Disease related to carnitine synthesis , transfer ease etc causes

A

Muscle cramping
Severe muscle weakness especially in exercise
Death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Fatty acid oxidation regulation

A

Malonyl coa can inhibit carnitine acyl transferase I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Goal of fatty acid oxidation

A

Break down of fatty acid produce ATP

Acetyl coa formes can enter citric cycle producing even more ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Beta oxidation pathway

A

Fatty acid converted to trans-enoyl -CoA by acyl Coa dehydrogenase
FADH2 PRODUCED

Trans-enoyl -coa converted to L-B-hydroxylacyl-CoA by enoyl coa hydratase

l-b-hydroxyacyl-COa converted to B-ketoacyl-CoA by B-hydroxyacyl-coa dehydrogenase
NADH PRODUCED

B-ketoacyl-CoA converted to acetyl-coa and fatty acids (less 2 carbons)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

ATP production per cycle of fatty acid oxidation

A

1 NADH
1 FADH2
1 Acetyl coa which goes to citric cycle

So that’s 2.5+1.5+10= 14 ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Do you use ATP during fatty acid activation?

A

Yes 2 ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Goal of fatty acid oxidation in peroxisomes

A

Breakdown of very long fatty acids (more than 22 carbons)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

X- adrenoleucodystrophy

A

Disease due to defect of ALD protein transport which lead to accumulation of long chain fatty acids because they can’t get to peroxisomes.

They destroy myelin and lead to death by 10 yo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Zellweger syndrome

A

Defect in peroxisome preventing breakdown of long chain fatty acid
Liver, kidney and muscles abnormalities
Death by 6yo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Products of odd chain fatty acid alpha oxidation

A

Proprionyl CoA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Fate of propionyl from odd fatty acid alpha oxidation

A

Peopionyl Coa converted to succinyl coA thanks to vitB12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Oxidation of monounsaturated fatty acid

A

enoyl coa isomerase convert the unsaturated fatty acid with cis configuration to trans enoyl coa

The rest of oxidation continue as usual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Oxidation of polyunsaturated fatty acids

A

2,4 dienoyl coa reductase convert the 2,4 dienoyl coa to cis enoyl coa ( monounsaturated)

Enoyl coa isomerase convert cis enoyl coa to trans enoyl coa.

Rest of oxidation continue as usual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Alpha oxidation location

A

Peroxisomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Oméga oxidation

A

Starts at methyl group
Occurs in smooth ER for part of cyt p450 pathway
Médium chain length FAs
No energy produced
Produce dicarboxylic group which when processed by beta oxidation produce succinate and adipate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Precursors of fat production

A

Carbohydrate

Protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Location of de novo fatty acid synthesis

A

Cytosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Fatty acid synthesis committed step

A

Acetyl coa converted to Malonyl coa by Acetyl coa carboxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Intermediate used to transport acetyl coa into cytosol for fatty acid synthesis

A

Citrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Acetyl coa carboxylation step to form malonyl coa

A

Carboxy biotin intermediate give activated CO2 to acetyl coa to form malonyl coa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Fatty acid synthesis spiral

A

Acyl carrier protein ACP bien malonyl coa and acetyl coa

Formation of acetylACP and malonylACP

Condensation reaction

Réduction réaction

Dehydration reaction

Reduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Fatty acid oxidation carrier

A

Coa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Fatty acid synthesis carrier

A

ACP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Is there bicarbonate dépendance in fatty acid synthesis

A

Yes - carbon dioxide donor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Major lipid in body

A

Acylglycerols

52
Q

TGs synthesis precursors

A

L-glycerol 3 pi

Fatty acyl coa

53
Q

Source of l glycerol 3 pi

A

Dihydroxyacetone phosphate reduced to L glycerol 3 pi

In liver only, glycerol from TGs degradation can be act on by glycerol kinase to form glycerol 3 pi

54
Q

Reduction of dihydroxyacetone pi occurs in

A

Liver and adipose tissue

55
Q

Adipocyte Only take up Glucose in the presence of insulin

True or false

A

True

56
Q

Fatty acyl activation before TGs synthesis

A

FA activated by coa addition

Leads to fatty acyl coa synthesis

57
Q

TGs synthesis mechanism

A

2 fatty acyl coa added to glycerol 3 pi at carbon 1 and 2 by glycerol phosphate acyltransferase

Gives phosphatidic acid

Phosphatidic acid hydrolyzed by phsphatidate phosphatase and gives diacylglycerol

Diacylglycerol reacts with 3rd fatty acid and gives TG Via diacylglycerol acyltransferase

58
Q

Phospholipids structure

A

L glycerol 3 pi with 2 hydroxyl group estérifier to fatty acids
Last groups estérifies to phosphoric acid

59
Q

Major classes of phospholipids

A

Glycerol backbone

Sphingosine backbone

60
Q

Most abundant phospholipids in plants and animals

A

Phosphatidylcholine

Phosphatidylethanolamine

Phosphatidyl serine

61
Q

Phospholipase A1 act on ..

A

FA at carbon 1

62
Q

A2 phospholipase act at

A

FA at carbon 2 of phospholipid

63
Q

C phospholipase act at

A

Before phosphate of phospholipid

64
Q

D phospholipase act at

A

After phosphate of phospholipids

65
Q

Phospholipase A2 role

A

Releases arachidonic acid from phosphotidylinositol to produce PG

66
Q

2 strategies of phospholipid synthesis

A

Diacyglycerol formed like in TGs synthesis activated by CDP which can then be replaced on molecule by polar head group

Or

CDP already bound to head group
Head group activated transferred to diacylglycerol giving the phospholipid

67
Q

Phosphatidylinsolitol serves as reservoir of

A

Arachidonic acid

68
Q

Which one is more hydrophobic
A . Cholesterol
B. Cholesteryl ester

A

B

69
Q

2 major sources of cholesterol in body

A

Dietary cholesterol

Cholesterol synthesized in extrahepatic tissues

De Novo synthesis from liver

70
Q

Route for Dietary cholesterol to liver

A

Chylomicron remnants

71
Q

Route for cholesterol synthesized in extraaheparic tissues to liver

A

HDL route

72
Q

Major fate of cholesterol

A

Secretion of VLDL

cholesterol secreted in bile

Cholesterol converted to bile acids

73
Q

Major sites of cholesterol synthesis

A

Liver and intestine 80%

74
Q

Other sites of cholesterol synthesis

A

Adrenal cortex

Reproductive tissue LIKE OVARIES AND TESTES

75
Q

Biosynthesis of cholesterol

A

(I)
2 Acetyl CoA —> acetoacetyl CoA
Enzyme : thiolase

(II)
Acetoacetyl CoA + acetyl CoA —> HMG-CoA
Enzyme : HMG

(III)
HMG CoA —> mevalonate
Enzyme : HMG-CoA reductase
NADPH used , CoA released

3 steps later , squalene is formed

Squalene gives lanosterol which gives cholesterol

76
Q

2 forms of HMG CoA synthase isoenzymes

A

Cytosolic form for cholesterol synthesis

Mitochondrial form for ketone body synthesis

77
Q

Rate limiting step in cholesterol synthesis

A

HMG CoA reductase

78
Q

Is HMG CoA reductase reversible or irreversible

A

Irreversible

79
Q

Regulation of HMG CoA reductase

A

High cholesterol inhibits enzyme

Inactive When enzyme phosphorylated

HMG COA pi —-> HMG CoA
Done by phosphatase

Phosphatase activated by insulin and inhibited by glucagon

AMP kinase can give the inactive form

80
Q

How is cholesterol eliminated in humans

A

Conversion to bile acids and bile salts

81
Q

What drugs are used in high plasma cholesterol

A

Statins (atorvastatin, lovastatin, simvastatin)

82
Q

How do statins help in decreasing cholesterol level

A

Act as analog of HMG CoA and competitively inhibit HMG CoA reductase

83
Q

Where are bile salts synthesized

A

Liver

84
Q

Primary bile acids

A

Cholic acid

Chenodeoxycholic acid

85
Q

Bile acid found in largest amount in bile

A

Cholic acid

86
Q

Fate of primary bile acids

A

Converted to glycine or taurine

87
Q

Lipoproteins functions

A

Transport of fat soluble substance

88
Q

Type of lipoproteins

A

Chylomicrons

VLDL

LDL

HDL

89
Q

Lipid part of lipoproteins

A

Depends on type of lipoproteins

90
Q

Protein part of lipoproteins

A

Apolipoproteins

91
Q

Lipoproteins classification

A

HDL (33% protein )

LDL

IDL

VLDL

Chylomicrons (1-2% proteins )

92
Q

Functions of apoproteins

A

Structural Components

Enzyme cofactors

Ligands for interaction with lipoprotein receptors in tissues

93
Q

Major apo lipoprotein in HDL

A

APO- A1

also found in chylomicrons

94
Q

Major chylomicrons apo lipoproteins

A

Apo-B48

95
Q

Major LDL apo lipoproteins

A

Apo-B100

also found in VLDL

96
Q

Apo c2

A

Found in HDL, chylomicron’s and VLDL

Serve as cofactor for lipoproteins lipase

97
Q

Apo E

A

Found in chylomicron remnants , VLDL, IDL, HDL

Ligand used for interaction with tissue lipoprotein receptor

98
Q

3 major pathways of lipid transport

A

Exogenous pathway (dietary lipids to tissues )

Endogenous pathway ( lipids from liver to tissues )

Reverse cholesterol transport pthway ( cholesterol in tissues to liver )

99
Q

Lipids and proteins proportion in chylomicrons

A

High percentage of lipid

Low protein percentage

100
Q

Chylomicrons lipid transport pathway

A

Exogenous lipid transport

101
Q

Lipoprotein responsible for milky appearance of plasma after meal

A

Chylomicrons

102
Q

Iipoproteins responsible for transport of cholesterol to liver

A

Remnants of chylomicrons

103
Q

Chylomicron pathway

A

Chylomicron carry dietary fats

Chylomicron acquire apo CII and apo E from HDL

Chylomicron complex meet lipoprotein lipase and removal of TGs and chylomicrons remnants released

Chylomicron remnants transport cholesterol to liver where apo E binds receptor on liver for delivery

104
Q

Where can you find lipoprotein lipase

A

Anchored to capillary wall of tissues ( adipose, cardiac, skeletal)

105
Q

Is there LPL in liver ?

A

No

106
Q

VLDL function

A

Transport TAGs from liver to target tissues

107
Q

Endogenous pathway of lipid transport

A

B100 helps form export VLDL

VLDL get apo CII, apo E From HDL

VLDL interacts lipoprotein lipase producing LDL

LDL goes to tissue where B100 binds receptors

LDL gets into cell and deliver cholesterol

108
Q

IDL fate

A

Converted to LDL

Direct uptake by liver

109
Q

Primary carrier of cholesterol for delivery to tissues

A

LDL

With highest half life

110
Q

How is the uptake of LDL done ?

A

Receptor mediated endocytosis

111
Q

Cholesterol uptake fats

A

Cholesterol incorporated into membrane

Repression of cholesterol synthesis

Stimulate of cholesterol storage

Repression of LDL receptor synthesis

112
Q

Reverse cholesterol transport pathway

A

Nascent HDL from liver with low lipid level

HDL circulâtes in blood and picks up cholesterol

HDL goes back to liver with cholesterol

113
Q

Functions of HDL

A

Reservoir of apolipoproteins necessary for other lipoproteins

Uptake of cholesterol- excellent acceptors of cholesterol

114
Q

Enzyme responsible for estérification of free cholesterol

A

Lecithin cholesterol acyltransferase (LCAT)

115
Q

What happens if Chosteryl ester present in HDL

A

HDL can’t get back to cell

116
Q

How is damaged LDL called

A

OxLDL

117
Q

What happens if elevated oxLDL

A

Increased monocytes adhésion leading to Marcel phases engulfing the oxLDL by endocytosis => form FOAM cells

118
Q

Benefits of HDL

A

Absorbs most of cholesterol in extra hepatic tissues “cholesterol sponge”

Unloads CE to liver

Degrades oxLDL

119
Q

Does increase lipoproteins especially LDL can lead to atherosclerosis?

A

Yes

120
Q

Source of hormones

A

Cholesterol

121
Q

Dyslipoproteinemia

A

Abnormal lipoproteins in blood

122
Q

Primary dyslipoproteinemia

A

Hyper synthesis or hypodegradation of lipoproteins due to enzyme deficiency

123
Q

Secondary lipoproteinemia

A 
Complication of another conditions 
Like :
Extrahepatic obstruction 
Exogenous sex hormones (oral pill)
Steroids 
Diabetes mellitus
Biliary cirrhosis 
Hypothyroidism 
Alcohol consumption 
Obesity 
Thiozide diuretics
124
Q

Fredickson classification Of lipid disorders

A

Type I dyslipidemia

Type IIa dyslipidemia

Type IIb dyslipidemia

Type III

Type IV.

125
Q

Type I dyslipidemia

A

Decreased lipoproteins lipase
Increased TGs so increased chylomicrons

Cause :
pancreatitis (TGs obstruction)
Éruptive xanthomas
Lipemia retinalis

126
Q

Type IIa lipidemia ( familial hypercholesteremia)

A

Familial
Young death if homozygous ( less than 20)
LDL receptor gene defect or absent

LDL cholesterol increased

Causes :

127
Q

Type IV familial combined hyperlipidemia

A

Obesity and insulin resistance common

Nutrition And Metabolism (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions