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biochemistry > lipid metabolisam > Flashcards

lipid metabolisam Flashcards

1
Q

when does ketone body metabolism take place

A

starving

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2
Q

where does ketone metabolism takes place

A

liver

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3
Q

what is the reaction takes place while producing ketone bodies

A

liver converts excess CoA from beta oxidation of fatty acids into ketone bodies

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4
Q

what are the example of ketone bodies

A
  1. Acetone
  2. Acetoacetate
  3. 3-hydroxybutyrate
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5
Q

which tissues will use ketone bodies as a source of energy

A

extrahepatic tissues like brain muscles etc

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6
Q

why does liver cannot use ketone bodies as a source of energy

A

liver does not contain succinyl CoA acetoacetyl CoA transferase (Thiosphosase)

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7
Q

name which part in our body metabolize acetoacetate and beta hydroxybutyrate to acetyl CoA

A

cardiac and skeletal muscle and renal cortex

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8
Q

what is ketogenisis

A

biochemical process by which organisms produces ketone bodies

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9
Q

how ketone bodies are produced

A

by the breakdown of fatty acids

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10
Q

at what circumstances ketogenisis occur

A

fasting and hypoglycemia

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11
Q

exessive production of ketone bodies leads to a dangerous state known as

A

ketoacidosis

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12
Q

when will brain begin to metabolize ketone body

A

after a week of fasting ketones reach a concentration in blood high

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13
Q

where will ketogenesis occurs

A

in mitochondria of hepatocytes

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14
Q

when will ketogenesis occur

A

when excess acetyl-CoA accumulates in the fasting state

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15
Q

name the enzyme that produce HMG- CoA

A

3-Hydroxy 3-Methyle Glutaryl-CoA (HMG-CoA) synthase

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16
Q

HMG-CoA lyase breaks ____________ into ____________

A

HMG-CoA into acetoacetate

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17
Q

name the ketone body that produced as a minor side product formed non enzymatically

A

Acetone

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18
Q

if acetone is used as a fuel it leads to

A

strong odor (sweet or fruity) to the breath

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19
Q

what are the condition favoring ketogenesis

A

fasting
carbohydrate restrictive diets
starvation
prolonged intense exercise
untreated type 1 diabetes mellitus

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20
Q

ketone bodies are converted into __________ by extrahepatic tissues which then enters the ____________and oxidized in the mitochondria

A

acetyl CoA , citric acid cycle

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21
Q

in brain ketone bodies are also used to make acetyl CoA into

A

long chain fatty acids

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22
Q

why acetyl CoA is converted to LCFA in brain

A

LCFA cannot be obtained from blood ( cannot pass through blood brain barrier)

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23
Q

how ketone bodies are generated in patients with type 1 diabetes mellitus

A

glucose- high , no insulin , hormone sensitive triglyceride lipase (HSL) is active, beta oxidation is not inhibited

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24
Q

ketoacidosis in type 1 diabetes mellitus patients

A
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25
Q

ketoacidosis in type 2 diabetes mellitus patients

A

develop after an infection or trauma

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26
Q

how ketoacidosis is developed in alcoholics

A

chronic hypoglycemia present in chronic alcoholism favors fat release from adipose tissue

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27
Q

why utilization of ketone is slower in alcoholics even though liver increase the production of ketone bodies

A

alcohol is converted to acetate in the liver diffuses into blood and oxidize by muscle as an alternative source of acetyl CoA

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28
Q

ketoacidosis is characterized by

A

polyuria, dehydration, & thirst
CNS depression and coma
potential depletion of k+
decreased plasma bicarbonate
breath with a sweet or fruity odor due to acetone

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29
Q

what is the difference between normal ketosis and pathological condition

A

acetoacetate and beta hydroxybutyrate are formed aprox. equal quantites in normal and their ratio sift in pathology , beta hydroxybutyrate predominates

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30
Q

what is ketogenic diet

A

high fat, adequate-protein, low carbohydrate diet

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31
Q

ketogenic diet is used primarily to treat

A

difficult-to-control epilepsy (forces the body to burn fats rather that carbohydrate)

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32
Q

when will liver depends on fatty acid oxidation and synthesize ketone bodies

A

if there is very little carbohydrate

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33
Q

ketosis leads to

A

reduction of epileptic seizures

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34
Q

what are sphingolipids

A

imp constituent of cell membrane
similar structure to the glycerophospholipids have a hydrophilic region and 2 fatty acid derived hydrophobic tails

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35
Q

various classes of sphingolipids differ primarily in

A

nature of the hydrophilic region

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36
Q

give example of sphingolipids and their hydrophilic group

A

sphingomyelin: phosphorylcholine
cerebrosides: galactose or glucose
gangliosides : branched oligosaccharides

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37
Q

what is released when membrane is degraded and digested in endosomes after fusion with lysosome

A

spingolipids

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38
Q

what is the action of enzymes in lysosome

A

removes specific groups from individual sphingolipids

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39
Q

which is the x-linked recessive sphingolipidosis

A

fabry disease

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40
Q

what are the autosomal recessive sphingolipidoses

A

tay- sachs, Gaucher, niemann-pick

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41
Q

fabry is caused by mutation in the gene that encodes

A

lysomal enzyme alpha- galactose
(Ceramide trihexoside accumulates in the lysosomes)

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42
Q

symptoms of fabry diseases

A

*burning sensation in the hand which get worse with exercise and hot weather
*small, raised reddish- purple blemishes on skin(angiokeratomas)
*eye manifestation
*impaired arterial circulation and increased risk of heart attack or stroke
*enlargement of heart and kidney

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43
Q

what is the treatment for fabry disease

A

enzyme replacement therapy

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44
Q

what are the components of bile

A

watery mixture of organic and inorganic compounds

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45
Q

what are the composition of bile

A

water-97%
bile salt-0.7%
bilirubin-0.2%
fat- (cholesterol, fatty acids & lecithin)
inorganic salt-200 meq/l

46
Q

what are the important organic components of bile

A

phosphatidylcholine(pc), lecithin, and conjugated bile

47
Q

how is bile is secreated

A

directly from liver into duodenum through the common bile duct or stored in gall bladder

48
Q

how many carbons are there in bile acid and what are the other groups

A

24 carbon with 2 or 3 hydroxyl group and side chain that terminate in a carboxyl group

49
Q

what are the orientation of bile salt and acid

A

hydroxyl grp- alpha
methyl grp- beta

50
Q

describe the polarity of bile molecule

A

have both a polar and a nonpolar surface

51
Q

what is the function of bile

A

act as a emulsifying agent in the intestine
helping prepare dietary fat & other complex lipids for degradation of pancreatic enzymes

52
Q

what are the most abundant bile acids in human bile

A

cholic acid and chenodeoxycholic acid

53
Q

bile acids are synthesized in the liver by a _________ and _________ pathway

A

multistep, multiorganelle

54
Q

on what structure hydroxyl grps are inserted at a specific position

A

steroid structure

55
Q

how is bile salt acid synthesis from cholesterol

A

double bond of cholesterol B ring is reduced and hydrocarbon chain is shortened by 3 carbons, introducing a carbonyl grp at the end of the chain

56
Q

name primary bile acids

A

cholic acid (triol), chenodeoxycholic acid ( diol )
most common resulting compound

57
Q

the rate limited step in bile acid synthesis is the introduction of a

A

hydroxyl group at C7 of steroid nucleus by 7-alpha-hydroxylase

58
Q

name the enzyme that is an associated cytochrome p450 (CYP) monooxygenase with found only in liver

A

7-alpha-hydroxylase

59
Q

expression of cholesterol-7-alpha hydroxylase is upregulated and downregulated by

A

cholesterol
bile acid (cholic acid )

60
Q

why chenodeoxycholic and not cholic acid, can be used to treat gallstones

A

because decreasing bile acid synthesis via inhibition of cholesterol-7-alpha hydroxylase would supersaturate the stones even more

61
Q

Which receptor is stimulated with elevated levels of cholesterol in the liver

A

nuclear receptor liver X factor (LXR)

62
Q

LXR increases the transcription of

A

cholesterol -7-alpha hydroxylase

63
Q

name the nuclear receptor that activates on elevated level of bile acids

A

bile acid receptor ( BAR) or farnesoid X receptor (FXR)

64
Q

BAR will downregulate the transcription of

A

cholesterol-7-alpha hydroxlase

65
Q

the carboxyl group of bile acid is conjugated by amide bond to a molecule of either __________ or ________ before living liver

A

glycine or taurine (end product of cysteine metaboisam

66
Q

the new molecule after conjugation are called

A

glycocholic, glycochenodeoxycholic acids and taurocholic and taurochenodeoxycholic acid

67
Q

the ratio of glycine to taurine forms in the bile is

A

3/1

68
Q

which type of ionized bile salts are more effective detergent, why

A

conjugated one, because of their enhanced amphipathic nature

69
Q

which form of bile salts are found in bile

A

only the conjugated form

70
Q

individuals with genetic deficiencies in the conversion of cholesterol to bile are treated with

A

exogenously supplied chenodeoxycholic acid

71
Q

bile salt provides significant mechanism for cholesterol excretion, both as a

A

metabolic product of cholesterol & solubilizer of cholesterol in bile

72
Q

bile salt secreted into the intestine are efficiently __________&___________

A

reabsorbed and reused

73
Q

bile salt efficiently taken up from the blood by the hepatocytes via

A

an isoform of the cotransporter

74
Q

what binds with the bile salts and transport them through the blood

A

albumin

75
Q

how is secondary bile salts are forms

A

some bile salt from cycle is deconjugated the dehydroxylated

76
Q

the secondary bile salts are uptaken in the
_________ and subsequent return to liver as a

A

ileum
mixture of primary and secondary forms

77
Q

how much bile salt is secreted by liver daily and how much lost daily

A

30 g
0.5 g

78
Q

0.5 g that lost is synthesized from ___________ in the liver to replavce the lost amt

A

choleaterol

79
Q

name one bile acid sequestrants

A

cholestramine

80
Q

how bile acid sequestrants promote their excreation

A

they bind bile salt in the gut and prevent their reabsorption

81
Q

bile acid sequestrants are used in the treatment of

A

hypercholesterolemia

82
Q

how hypercholesterolemia treatment works

A

removal of bile salt relieves the inhibition on bile acid synthesis in liver thereby diverting additional cholesterol into that pathway
dietary fiber also binds bile salt and increases their excretion

83
Q

where and by what bile salts are exposed to bacterial modification b

A

in the colon by gut microbiome

84
Q

what are the secondary bile acid

A

deoxycholic acids from cholic acid
lithocholic acid from chenodeoxycholic acid

85
Q

how is secondary bile salts are produced

A

by dehydroxylate carbon 7

86
Q

a small proportion of these secondary bile acids are absorbed by the

A

colonic epithelium

87
Q

the movement of cholesterol from the liver into bile must be accomplished by the

A

simultaneous secretion of phospholipid and bile salts

88
Q

if cholesterol may precipitate in the gallbladder, leading to

A

cholesterol gallstone disease or cholelithiasis

89
Q

cholelithiasis is caused by a

A

decrease of bile acids in the bile

90
Q

choleolithiasis also may result from

A

increased secretion of cholesterol into bile with the use of fibrates to reduce cholesterol in blood

91
Q

example of fibrate

A

gemfibrozil

92
Q

what is the treatment method for cholelithiasis

A

laparoscopic cholecystectomy

93
Q

treatment for patients who cannot undergo surgery is

A

oral administration of chenogeoxycholic acid

94
Q

fatty acid synthesis is also known as

A

de novo synthesis (new synthesis from amphibolic compounds )
lipogenesis

95
Q

sites of fatty acid synthesis

A

liver, kidney, brain, lungs, mammary gland & adipose tissue

96
Q

organelle of fatty acid synthesis

A

cytosol

97
Q

which is the principal building block of fatty acid

A

acetyl CoA

98
Q

name the method of synthesis of saturated fatty acids from acetyl CoA that is primarily derived from glucose, and occurs in

A

de novo synthesis
cytoplasm

99
Q

elongation of fatty acids are and occurs in

A

acetyl fragments are added to the existing FAs
occurs in cytoplasm and mitochondria

100
Q

double bonds introduced into the FAs are called and occurs in

A

desaturation of fatty acids
microsomes

101
Q

what all steps of FA synthesis occur in mitochondria

A

catabolism by beta-oxidation
some chain lengthening

102
Q

chain lengthening and introduction of double bonds occur in

A

endoplasmic reticulum

103
Q

anabolism & formation of acyl-CoA occur in `

A

cytosol

104
Q

the process in which C2 acetyl CoA converted to C16 palmitic acid is

A

De Novo synthesis

105
Q

major FA synthesised in denov is

A

palmitic acid

106
Q

which is the source of carbon atoms in FA synthesis

A

Acetyl CoA

107
Q

NADPH id the source of _________ in FA synthesis

A

reducing equivalents

108
Q

source of energy in FA synthesis

A

ATP

109
Q

source of acetyl CoA is

A

aerobic glycolysis
FA oxidation

110
Q

source of NADPH

A

HMP shunt pathway
malic enzyme (NADP malate dehydrogenase)
the extra

biochemistry (12 decks)

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