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MCB II Block 3 > Mobilization and degradation of stored fat > Flashcards

Mobilization and degradation of stored fat Flashcards

1
Q

describe the storage of energy in regards to lipids

A

they can store a ton of energy. hydrophobic helps them pack a lot. stable molecule

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2
Q

describe how lipids insulate from enviornment

A

low thermal conductivity
high heat capacity AKA it can absorb heat
mechanical protection AKA it can absorb shock

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3
Q

what stimulates lipolysis

A

glucagon or epinephrine

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4
Q

durling lipolysis what is inhibited

A

glycolysis

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5
Q

when epinephrine binds to its receptor and activates cAMP, what is phosphorylated

A

hormone sensitive lipase

perilipin

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6
Q

what phosphorylates hormone sensitive lipase

A

protein kinase A

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7
Q

free fatty acids go into blood and what do they bind

A

albumin

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8
Q

draw out mechanism of epinephrine causeing release of fatty acid

A

pg 6

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9
Q

what is albumin

A

FFA carrier

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10
Q

fatty acids in the tissue undergo what in the mitochondria

A

ß oxidation

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11
Q

free fatty acids in blood come from degradation of

A

TAGs in adipocytes

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12
Q

in order to get fatty acid inside cell, what protein is used

A

CD36

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13
Q

once FFA is inside cell how is it activaed

A

forms thioester bond to form CoA derivitive

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14
Q

what is function of Carnitine

A

allows moving long chain fatty acids to matrix of mitochondria

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15
Q

once long chain fatty acids are in mitochondria, they are broken down via what process

A

ß oxidation

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16
Q

write out the fatty acid activation in the cytosol

A

pg 8

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17
Q

is fatty acid activation exergonic or endergonic

A

exergonic

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18
Q

what is the end result of fatty acid activation in cytosol

A

Acetyl-CoA activated with thioester bond

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19
Q

draw out the metabolism of fatty acids chart including the size class, number of carbons, site of catabolism, membrane transport for: short, medium, long, very long, and brained fatty acids

A

pg 9

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20
Q

what is Carnitine needed for

A

to transport long chain fatty acids into mitochondria

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21
Q

Carnitine transport long chain fatty acids in what form

A

carnityl ester

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22
Q

do medium chain fatty acids need Carnitine to transport into mitochondria

A

no

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23
Q

what catalyses the reaction b/w long chain fatty acids and Carnitine

A

carnitine palmitoyltransferase I

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24
Q

once inside the micotchondria, what happens to the fatty acid and carnitine

A

carnitine palmitoyltransferase II catalyses rxn which releases carnitine

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25
Q

draw out the mechanism for long chain fatty acid transport into mitochondria

A

pg 10

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26
Q

what does the enzyme carnitine acetyltransferase (CAT) do in the mitochondrial matrix

A

reconvert short- and medium-chain acyl-CoAs into acylcarnitines using intramitochondrial carnitine.

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27
Q

what two organs can export carnitine into blood

A

liver & kidney

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28
Q

carnitine is synthesized from what AA

A

lysine & methionine

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29
Q

what regulates carnitine system

A

peroxisome proliferator-activated receptors [26] and hormones such as insulin, glucagon, norepinephrine, thyroid hormone, dopamine and androgens.

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30
Q

draw out protein degradation to make carnitien

A

pg 11

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31
Q

ß oxidation is length

A

specific

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32
Q

draw out the ß oxidation of FA-CoA

A

pg 13 (left)

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33
Q

ß oxidation of FA-CoA releases

A

2 carbons

acetyl CoA

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34
Q

in the four step proess for ß oxidation of FA-CoA, name the type of reactions for first four steps

A

dehydrogenation
hydration
dehydrogenation
thiolysis

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35
Q

what is the total energy yeild of palmitic acid

A

106 ATP

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36
Q

how many carbons is palmitic acid

A

16

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37
Q

what are the 3 final products from beta oxidation of palmitic acid

A

FADH2
NADH
Acetyl CoA

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38
Q

pyruvate carboxylase is allosterically activated by

A

Acetyl CoA

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39
Q

what is used as the sensor to connect gluconeogenesis and beta oxidation

A

pyruvate carboxylase

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40
Q

gluconeogenesis requires how much ATP

A

11 moles

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41
Q

draw out pyruvate carboxylase and its role in gluconeogenesis and beta oxidation

A

pg 17

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42
Q

oxidation of fatty acids to CO2 requires more O2 than

A

aerobic carbohydrate oxidation

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43
Q

what is relationship b/w reduced substrate and O2

A

the more heavily reduced a substrate, the more O2 must be consumed to produce equal amounts of CO2

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44
Q

what are the only oxidaton products of beta oxidation

A

FADH2 & NADH

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45
Q

what does RQ stand for

A

respiratory quotient

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46
Q

RQ=

A

CO2 produced/ O2 consumed

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47
Q

compare RQ for glucose & Stearate

A

2 glucose: 1.0

2 Stearate: 0.71

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48
Q

what is RQ of carbohydrates

A

1

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49
Q

what is RQ of fats

A

.71

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50
Q

what is RQ of proteins

A

.9

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51
Q

a smaller RQ means

A

more oxygen is being consumed

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52
Q

RQ greater than 1 means

A

anaerobic respiration is occurring

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53
Q

what controls ß oxidation of fatty acids

A

hormones
malonyl CoA inhibits CPTI
rate of ATP in ETC

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54
Q

draw out regulation of ß oxidation

A

pg 20

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55
Q

what blocks malonyl CoA

A

low energy charge (AMP?)

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56
Q

what kind of bonds to all unsaturated fatty acids have

A

cis

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57
Q

draw out example of saturated and unsaturated fatty acid

A

pg 21

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58
Q

how does the body oxidize cis unsaturated FA

A

first have to get rid of cis bond and make it trans: 1st oxidation
then normal oxidation

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59
Q

1st oxidation of cis unsaturated FA yields

A

FADH2 & trans bond

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60
Q

trans fatty acids are:

A

deadly!

cause high LDL cholesterol and cardiovascular disease

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61
Q

describe structure of trans fat

A

trans double bond
compared to unsaturated which has cis double bond
and saturated has no double bonds

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62
Q

biotin allows conversion of propionyl CoA to

A

D-methylmalonyl CoA.

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63
Q

odd number fatty acid oxidation forms

A

propionyl CoA

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64
Q

vitamin B 12 allows for isomerization of L-methylmalonyl CoA to

A

succinyl CoA

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65
Q

draw out the mechanism of odd numbered fatty acid

A

pg 25

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66
Q

what carbon does ß oxidation occur on

A

3rd

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67
Q

where does α oxidation occur

A

C2

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68
Q

where does w oxidation occur

A

methyl end of fatty acid

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69
Q

why does peroxisomal fatty acid oxidation occur

A

chain shortening of very long chain fatty acids

70
Q

if there is a deficiency in α oxidation, what disease

A

Refsum disease

71
Q

why is fatty acid oxidation done in mitochondria

A

b/c product is Acetyl CoA which is fuel of TCA. TCA happens in mitochondria

72
Q

describe general structure of lipid

A

carboxyl group with hydrocarbon chain

73
Q

explain how pts with diabetes have accumulation of fatty acids in blood

A

insulin receptor doesn’t work so increase in epinephrine response and mroe fatty acid in blood (pg 6)

74
Q

what is the destination of glycerol?

A

to liver to produce glucose, gluconeognesis? (i think this is what he said)

75
Q

what is the most abundant protein in blood

A

albumin

76
Q

babies do not have shuttle for

A

long chain fatty acid

77
Q

what fat does milk contain

A

short and medium chain fatty acid - doesn’t have long chain b/c babies don’t have shuttle for long chain

78
Q

if pt only has one kidney what will you need to give him

A

caratine supplement

79
Q

where is isoleucine processed

A

muscle cells

80
Q

if you accumulate acetyl coA what happens to ß oxidation

A

it stops

81
Q

what does it mean that acetyl coA makes ketone bodies in regards to ß oxidation

A

they release coenzyme A which is used to keep ß oxidation moving

82
Q

stearate is an example of a

A

fatty acid

83
Q

name two examples of branched fatty acids that would need to undergo α oxidation

A

Phytanic & Pristanic

84
Q

why can’t phytanic acid undergo normal beta oxidation

A

it is branched

85
Q

draw out the alpha oxidation of phytanic acid

A

pg 27

86
Q

what is the first step in alpha oxidation of phytanic acid

A

alpha carbon hydrolxylated

87
Q

what is needed to take off alpha carbon of phytanic acid in alpha oxidation

A

vitamin C

88
Q

how many carbons is phytanic acid

A

20

89
Q

once a carbon is taken off of phytanic acid, it is now 19 carbon acid called

A

pristanic

90
Q

what kind of oxidation does pristanic acid undergo

A

three rounds of ß oxidation

91
Q

where are the three rounds of ß oxidation for pristanic acid taking place

A

peroxisome

92
Q

where in the cell does α oxidation take place

A

peroxisome

93
Q

if there is a defiency of phytanic acid oxidase enzyme, which is needed for α oxidation, what is the disease?

A

refsum disease

94
Q

what are the symptoms of refsum disease

A

Peripheral polyneuropathy, cerebellar ataxia,retinitis pigmentosa, and Ichthyosis (rough, dry and scaly skin)are the major clinical components

95
Q

if ß oxidation is impaired what takes over

A

w oxidation

96
Q

what is the first step in w oxidation

A

w hydroxylation of fatty acid

97
Q

what catalyzes the first step: w hydroxylation of fatty acid, in w oxidation?

A

w hydroxylase (CYP4A11)

98
Q

what is the human name of w hydroxylase specific for w oxidation

A

CYP4A11

99
Q

draw out w oxidation

A

pg 28

100
Q

where are very long chain fatty acids degraded

A

peroxisome

101
Q

draw out steps of very long chain fatty acid degradation

A

pg 29

102
Q

what are products of very long chain fatty acid degradation

A

Acetyl-CoA, NADH, H2O2, MCFA-CoA

103
Q

when does very long chain fatty acid degradation stop

A

at 4 to 6 carbons

104
Q

what does COT stand for

A

carnitine octanoyl transferase

105
Q

what does CAC stand for

A

carnitine acyl carrier

106
Q

what does MCAD stand for

A

medium chain acyl CoA dehydrogenase

107
Q

MCAD deficiency, what does it impair

A

ß oxidation of medium chain fatty acid

108
Q

how does MCAD deficiency present

A

hypoglycemia
dicarboxylic aciduria
no ketone bodies

109
Q

what does CAT deficiency stand for

A

carnitine acylcarnitine translocase deficiency

110
Q

CAT deficiency impairs what

A

ß oxidation of long chain fatty acids

111
Q

how does CAT deficiency present

A

muscle pain

myoglobinuria after exercise

112
Q

triglycerides are packaged into

A

lipoproteins

113
Q

what is hypertriglyceridemia?

A

fasting triglycerides more than 200 mg/dl

114
Q

hypertriglyceridemia is correlated with an increased risk of

A

cardiovascular disease

115
Q

if there are extreme elevations of triglycerides you might get

A

acute pancreatitis

116
Q

draw chart of what happens if beta oxidation is impaired by MCAD

A

pg 31

117
Q

draw chart of what happens if beta oxidation is impaired by carnitine

A

pg 32

118
Q

fatty acid use inhibits aerobic use of

A

glucose

119
Q

Ackee fruit contains

A

hypoglycin

120
Q

hypoglycin is a toxin that does what

A

inhibits fatty acyl-CoA dehydrogenase for short & medium chain fatty acids

121
Q

describe what happens in jamaican vomitting sickness

A

person eats ackee fruit which contains hypoglycin
vomitting
convulsions, coma, death

122
Q

what happens to free fatty acid levels after consumption of ackee fruit

A

they rise b/c of increased ß oxidation

123
Q

what is being excreted in urine after consumption of ackee fruit

A

dicarboxylic acids b/c of w oxidation

124
Q

what are symptoms of defective carnitine acyltransferase

A 
muscle cramps during exercise
severe weakness
hypoketosis
hypoglycemia
death
125
Q

what is treatment of defective carnitine acyltransferae

A

diet of medium chain fatty acids

126
Q

in adolescent/adults why is there red urine in pts with defective carnitine acyltransferase

A

myoglobinuria (myoglobin in urine) brought on by exercise/fasting

127
Q

when might there be secondary carntine deficiency

A

pregnancy, esp. second half
malnutrition, esp with vegetarian diet
severe infection, trauma, burn
ppl underoing hemodialysis

128
Q

what does MCAD stand for

A

medium chain acyl-CoA dehydrogenase deficiency

129
Q

what are symptoms of MCAD

A

preprandial (pre-feeding) irritability, drowsiness sweating, jitteriness, seizures, enlarged liver

130
Q

what would lab data show for MCAD

A

low plasma pH, low ketones, elevated dicarboxylic acids (eg: OAA), elevated fatty acids (FA’s), hypoglycemia

131
Q

what chrom. is MCAD gene on

A

1

132
Q

what happens to MCAD gene specifically in MCAD

A

substitute G for A @ residue 985 on chrom. 1

133
Q

ketone bodies are dimers of

A

acetyl CoA

134
Q

FA’s liberated from TG stores via ß oxidation produce

A

acetyl CoA

135
Q

what is the second product of lipolysis

A

glycoerol

136
Q

ketone bodies produced in the liver are int he form of

A

hydroxybutyrate & acetoacetate

137
Q

what controls the ratio of hydroxybutyrate & acetoacetate

A

cellular NAD+/NADH ratio

138
Q

how does NAD+/NADH contorl ratio of hydroxybutyrate & acetoacetate

A

NADH provides the reducing powet for the conversion of acetoacetate to ß-hydroxybutyrate

139
Q

ß-OH butyrate stands for

A

hydroxybutyrate

140
Q

ß-OH butyrate is not a true

A

ketone body

141
Q

formation of ketone bodies is coordinated with the production of

A

glucose vs. gluconeogenesis

142
Q

is ketogenesis during fasting or fed state

A

fasting

143
Q

describe ketogenesis

A

gluconeogenesis

fatty acid breakdown → ketone bodies

144
Q

ketone bodies can provide up to how much of brain’s energy requirements

A

60%

145
Q

how are ketone bodies transported across BBB

A

monocarboxylate transporters

146
Q

what does MCT-1 stand for

A

monocarboxylate transporter

147
Q

what is rate limiting step for brain cells to metabolize ketone bodies

A

shortage of MCT-1

148
Q

what happens in starvation or ketogenic diet to brain?

A

increase in MCT-1

149
Q

where does cholesterol biosynthesis occur

A

cytosol

150
Q

where does ketogenesis occur

A

mitochondria

151
Q

draw out ketogenesis

A

pg 44

152
Q

draw out cholesterol biosynthesis

A

pg 44

153
Q

where does reduction of acetate take place

A

cytosol

154
Q

reduction of acetate depends on what ratio

A

NADH/NAD+

155
Q

what is the regulation of cholesterol biosynthesis

A

there is no direct allosteric regulation, the regulation is the rate of acetyl-coa production

156
Q

what is the rate limiter of cholsterol biosynthesis

A

HMG-CoA synthase

157
Q

what induces HMG-CoA synthase

A

fasting
fat feeding
insulin deficiency

158
Q

what cells prefer to use ketone bodies over fatty acids

A

intestinal cells & adipocytes

159
Q

what are the advantages of ketogenesis

A

continuous FA oxidation in liver
other tissues can use ketone bodies and spare glucose
brain can use

160
Q

what cells cannot use ketogenesis

A

liver & RBC

161
Q

in plasma what happens to acetoacetate

A

spontaneous decarboxylation → volatile acetone (“true ketone”)

162
Q

draw out ketogenesis

A

pg 46

163
Q

what is normal ratio b/w β-hydroxybutyrate & Acetoacetate

A

4:1

164
Q

why can’t the liver metabolize acetoacetate

A

it doesn’t have thiophorase (Succinyl CoA: acetoacetate CoA transferase)

165
Q

draw out ketone catabolism

A

pg 47

166
Q

once ß OH butyrate enters cytosol,

A

oxidized to acetoacetate

167
Q

what is the product of ketone catabolism

A

actyl-CoA

168
Q

draw out ketogenesis and catbolism from liver to muscle

A

pg 48

169
Q

what tissue is always using ketone bodies

A

muscle & heart

170
Q

why do diabetics have ketoacidosis

A

they don’t have enough insulin, so they have too much EPI & glucagon, which means they do too much lipolysis, → too much free fatty acids → hepatic output of ketone bodies → ketoacidosis

171
Q

if there is Vitamin B12 deficiency affect what organ

A

brain

MCB II Block 3 (6 decks)

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