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MCB II Block 3 > Fatty Acid: Synthesis & Storage > Flashcards

Fatty Acid: Synthesis & Storage Flashcards

1
Q

where does fatty acid synthesis take place

A

cytosol

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2
Q

for synthesis of fatty acids, where does it obtain the carbons for it

A

shuttled from mitochondria via citrate

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3
Q

triacylglycerol synthesis is regulated by

A

insulin

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4
Q

if there is a lack of insulin (diabetes), what does it result in regarding fatty acid synthesis

A

increased lipolysis
increased fatty acid oxidation
failure to synthesize fatty acids

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5
Q

draw out the pathway of how insulin influences fatty acid synthesis and what direction it goes without insulingp

A

pg 5

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6
Q

what is the primary FA factory

A

hepatocyte

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7
Q

in FA synthesis how much ATP is contained in each acetyl CoA unit

A

10

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8
Q

besides liver, what else participates in FA synthesis

A

adipocyte

skin

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9
Q

glycolysis provides what 2 essential compounds for lipogenesis

A

Dihydroxyacetone-P

Pyruvate

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10
Q

what is a major carbon source for lipogenesis

A

glucose

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11
Q

what is function of Dihydroxyacetone-P

A

this becomes the scaffold that receives 3 fatty acids & becomes triacylglycerol – also TAG

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12
Q

what is function of pyruvate in lipogenesis

A

after conversion to acetyl-CoA and citrate – provides building blocks for fatty acid synthase in the cytosol

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13
Q

Acetyl CoA is shuttled from mitochondria to cytosol via

A

citrate

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14
Q

what is Acetyl CoA produced from

A

AA’s or carbohydrate

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15
Q

what breaks down citrate in cytosol

A

ATP-Citrate lyase

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16
Q

draw out pathway of citrate leaving and entering mitochodnria/cytosol

A

pg 7

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17
Q

pyruvate is decarboxylated to create

A

Acetyl CoA

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18
Q

pyruvate is diverted and carboxylated to produce

A

pyruvate carboxylase

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19
Q

Acetyl CoA + OAA with citrate synthase =

A

citrate

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20
Q

cell’s high energy charge inhibits

A

Isocitrate dehydrogenase

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21
Q

if Isocitrate dehydrogenase is inhibited, what happens

A

citrate accumulates and is exported via citrate shuttle

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22
Q

draw out the “balancing act” of forming citrate in mitochondria from pyruvate

A

pg 8

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23
Q

why is ATP needed for citrate lyase to break citrate into acetyl CoA & OAA

A

citrate is stable & energy needed to break bonds

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24
Q

pyruvate recycling produces add’l

A

NADPH

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25
Q

if there is insulin and enough energy you will produce

A

fat

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26
Q

what pathway is needed to produce fat

A

PPP (pentose phosphate pathway)

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27
Q

what is rate limiting step of fatty acid synthesis

A

ACC (acetyl CoA Carboxylase)

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28
Q

what enzymes require biotin

A

ACC
pyruvate carboxylase
propinyl coA

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29
Q

prostaglands are

A

hormones

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30
Q

prostaglands require

A

fatty acid

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31
Q

what kind of fatty acid do we need from diet

A

omega 6

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32
Q

to accumulate citrate have to stop or slow down

A

TCA cycle

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33
Q

How many carbons in Lauric acid

A

12 and 0 unsaturated

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34
Q

how many carbons in Myristic acid

A

14 and 0 unsaturated

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35
Q

how many carbons in Palmitic acid

A

16 and 0 unsaturated

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36
Q

how many carbons in Stearic acid

A

18 and 0 unsaturated

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37
Q

what are the two main ways NADH is produced

A

PPP

malic enzyme

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38
Q

describe how PPP makes NADH

A

The oxidative component of the pentose phosphate pathway two dehydrogenases allows the production of NADPH

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39
Q

describe how malic enzyme makes NADH

A

Malic enzyme recycles malate into pyruvate and in the process produces NADPH

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40
Q

production of NADPH is essentia for

A

fatty acid biosynthesis

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41
Q

what are the two dehydrogenases in PPP that produce NADPH

A

glucose 6 phosphate dehydrogenase and 6-phopogluconate dehydrogenase

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42
Q

what is a three carbon intermediate of acetyl coA

A

malonyl CoA

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43
Q

when enzyme is needed for acetyl coA → malonyl coA

A

Acetyl-CoA carboxylase

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44
Q

carboxylation requires

A

biotin

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45
Q

biotin deficiency has what symptoms

A

gastrointestinal upset, dermatitis, alopecia, paraesthesia and muscleache.

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46
Q

what is the major regulatory step to produce fatty acids

A

acetyl coa → malonyl coa

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47
Q

acetyl coa → malonyl reaction, what is needed

A

biotin
CO2
ATP

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48
Q

what are the 4 enzymes that require biotin

A

propionyl coenzyme A (CoA) carboxylase (PCC), pyruvate carboxylase (PC), β-methylcrotonyl CoA carboxylase (β-MCC), and acetyl CoA carboxylase (ACC).

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49
Q

what interfere with ingestion of biotin

A

avidin

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50
Q

where is avidin found

A

raw egg whites

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51
Q

what is allosteric activatory of acetyl CoA carboxylase?

A

citrate

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52
Q

what is allosteric inhibitor of acetyl CoA carboxylase?

A

palmitoyl CoA

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53
Q

how does citrate promote activity of acetyl coA carboxylase

A

induction of polymerization and gene expression

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54
Q

how does Palmitoyl-CoA inhibit activity of acetyl CoA carboxylase?

A

inhibits activity and induction via promoting depolymerization

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55
Q

what does by AMP-protein kinase (AMPK) do to acetyl coA carboxylase

A

inactivates

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56
Q

how does AMP protein kinase inactivate Acetyl CoA carboxylase

A

phosphorylation

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57
Q

with high levels of ATP what happens to acetyl CoA Carboxylase

A

Dephosphorylation, activated

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58
Q

describe the structure of fatty acid synthase

A

solid-state dimer of two multi-function monomers

symmetrical

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59
Q

Acyl carrier protein’s function holds growing acyl group with what bond?

A

thioester bond

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60
Q

with how many carbons does fatty acyl chain grow

A

2

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61
Q

how many carbons is palmitate acid

A

16

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62
Q

what donates carbons for growing chain of fatty acid

A

activated malonate

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63
Q

draw comparison of oxidative degradation & FA synthesis

A

pg 16

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64
Q

there is no free intracellullar palmitate, it exsits as

A

palmitoyl-CoA

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65
Q

what inhibits translocation of fatty acids to mitochondria

A

malonyl CoA

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66
Q

when lipogenesis is happening what does malonyl CoA do to ß oxidation

A

shut it down

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67
Q

where are FA elongated

A

ER

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68
Q

what is carbon source for FA elongation

A

malonyl CoA

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69
Q

what is used for reducing power for FA elongation

A

NADPH

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70
Q

what is the major difference b/w elongation of fatty acids and synthesis

A

in elongation: growing acyl chain is joined by thioester bonds to CoASH instead of ACP

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71
Q

what are two fatty acids we cannot synthesize

A

18:2 linoleic (Ω-6) and& 18:3 linolenic (Ω-3)

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72
Q

mammals cannot insert double bonds beyond what point

A

C9-10

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73
Q

draw out the Desaturation of a fatty acid by fatty acyl-CoA desaturase

A

pg 21

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74
Q

where does desaturation of FA take place

A

lumenal side of smooth ER

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75
Q

describe characterisitc of cytochrome P450 enzymes

A

located in themembrane endoplasmic reticulum and uses NADPH and O2.

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76
Q

fatty acyl-CoA desaturase is a member of what family

A

cytochrome P450

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77
Q

linoleic acid gives rise to

A

arachidonic acid

78
Q

what is a vital component in the water barrier in skin

A

ceramide

79
Q

in making a FA, after a desaturation then what

A

elongation of 2 Cs then another desaturation

80
Q

arachidonic acid is needed as a major component of

A

water barrier in skin

81
Q

what does PUFA stand for

A

polyunsaturated fatty acids

82
Q

essential fatty acids are

A

Ω-3 and Ω-6

83
Q

what is Ω-3

A

linolenic acid

84
Q

what is Ω-6

A

linoeic acid

85
Q

what is Alpha(α)-linolenic acid converted to

A

eicosapentaenoic acid & docosahexaenoic acid

86
Q

the final step in docosahexaenoic acid synthesis is

A

peroxisomal β-oxidation to remove the 2-carbon acetyl-CoA from the 24:6 fatty acid called tetracosahexaenoic acid

87
Q

what enzymes allow alpha linoleic acid to convert to EPA & DHA?

A

microsomal ER enzymes

88
Q

what cells synthesize triglycerides

A

basically all of them

89
Q

what activate free FA

A

CoASH

90
Q

TAG stands for

A

triacylglyceride

91
Q

TAG synthesis usually begins with

A

glycerol

92
Q

what is first step to make TAG

A

glycerol phoshporylated

93
Q

what enzyme phoshporylates glycerol in first step to make TAG

A

glycerol kinase

94
Q

after glycerol is phosphorylated, what happens in TAG synthesis

A

activated fatty acids serve as substrates for fatty acid addition

95
Q

in adipose tissue there is no expression of

A

glycerol kinase

96
Q

since there isn’t glycerol kinase in adipose tissue, what is used to make Tag

A

DHAP (from glycolysis)

97
Q

draw pathway for TAG synthesis in other tissues, adipocytes, and intestinal enterocytes

A

pg 24

98
Q

insulin stimulates conversion of excess glucose to

A

glycogen & TAG

99
Q

what does VLDL stand for

A

very long density lipopotrein

100
Q

what enzyme is needed to breakdown TAG

A

lipoprotein lipase

101
Q

during fasting, TAGs assembled in liver are loaded into

A

VLDL particles

102
Q

where does VLDL assembly begin

A

RER

103
Q

what does APO B-100 do

A

assembles core of phospholipids

mediate TG delivery at specific tissue destinations

104
Q

VLDL is seceted into blood for what purpose

A

tissues have access to cholesterol and fatty acids

105
Q

LPL stands for

A

lipoprotein Lipase

106
Q

LPL is attached to

A

capillary wall

107
Q

what activates LPL

A

apoprotein CII

108
Q

what inhibits LPL

A

Apo CIII

109
Q

TAG’s are hydrolyzed by

A

LPL

110
Q

inside cells fatty acids are activated with

A

CoASH

111
Q

what happens to FA to store them as TAGs

A

esterified

112
Q

what is the difference b/w VLDL & chylomicrons?

A

chylomicrons comes from the lipids in the diet, that cholesterol and TAGs while VLFL are TAGS and cholesterol produced by the liver.
so basically chylomicrons = diet
VLDL = we make it

113
Q

what holds LPL to capillary wall

A

heparan sulfate tether

114
Q

LPL requires activation by

A

Apoprotein CII

115
Q

how does NADH production make sense? how does it help us?

A

needed to fuel fatty acid biosynthesis

116
Q

describe acetyl coa regulation

A

acetyl coA needs to accumulate but not so much to inhibit pyruvate DH
needs careful regulation

117
Q

biotin deficiency symptoms related to

A

fatty acid synthesis

propionyl coA

118
Q

propionyl coA is important for the

A

brain

119
Q

what does enzyme do to acetyl coA carboxylase

A

activates by dephosphorylating

120
Q

acetyl coa carboxylase when it is monomer vs polymer when is it active vs. inactive

A

monomer: inactive
polymer: active

121
Q

FAS monomers contain covalently bound

A

phosphopantotheine

122
Q

phosphopantotheine is what

A

vitamin

123
Q

phosphopantotheine is bound to what residuc of ACP on FAS (fatty acid synthase)

A

serine

124
Q

phosphopantotheine is attached to the FAS protein itself via

A

serine

125
Q

tRNA occupies t and a site. on a site have free amino group b/c using carboxylic group. amino group nucleophilic attack that will attack ester bond in t site to form peptide bond. moves to a site and become t site (not sure if he is saying t or p)
first is terminal last one removed is ???

A

help

126
Q

ACP site and cysteine site

A

moved from ACP to other site ???? pg 14

127
Q

FA biosynthesis and ß oxidation

A

are similar, basically just opposite

128
Q

Acetyl-CoA + 7 Malonyl-CoA + 14 NADPH + 14 H+yields

A

Palmitate + 7 CO2 + 14 NADP+ + 8 CoASH;

add 8 ATP (for citrate lyase)

129
Q

Palmitate + 7 CO2 + 14 NADP+ + 8 CoASH;

add 8 ATP (for citrate lyase) comes from

A

Acetyl-CoA + 7 Malonyl-CoA + 14 NADPH + 14 H+yields

130
Q

The cytosolic produced 16 carbons, palmitoyl CoA is translocated to the ER so elongase enzyme activity extends it to 18 carbon units called

A

estearic acid.

131
Q

draw out Oxaloacetate & acetyl coa crossing cytosol

A

pg 9

132
Q

look at sequence of events during synthesis of fatty acid

A

pg 14

133
Q

omega 6 in diet comes in what form

A

linoelic acid (omega 6)

134
Q

desaturase is located where

A

ER

135
Q

ALA stands for

A

Alpha(α)-linolenic acid

136
Q

VLDL is from liver and equivalent to

A

chylomicron

137
Q

protein in chylomicron to help is

A

Apoprotein B 48

138
Q

protein in VLDL to help is

A

Apoprotein B 100

139
Q

VLDL is source of

A

LDL

140
Q

LDL comes from

A

VLDL

141
Q

chylomicrons are present in what state

A

well fed

142
Q

VLDL are present in what state

A

fasting

143
Q

Apo CIII is

A

inhibitor of lipoprotein lipase

144
Q

pts whoh ave GOF of Apo CIII what happens

A

packing of LPL is inhibited. it interferes with assembly of triacylglycerides in VLDL and it goes back to liver and they start to get liver problems and have fatty liver which is precursor to diabetes type II

145
Q

how is glucose trapped and controlled in liver without insulin signaling (how do we control glucokinase?)

A

glucokinase is trapped in the nuclei

146
Q

write out the comparison/contrast of synthesis and degradation & understand

A

pg 17

147
Q

when adipocytes are too big what happens

A

they attract attention of marophages which interfere with insulin signaling

148
Q

what is the initial acceptor of fatty acids during TAG synthesis?

A

Glycerol-3-phosphate

149
Q

during the well fed state what do liver and adipoctyes use to produce glycerol-3-phosphate

A

glycolysis intermediate: dihydroacetone phosphate (DHAP)

150
Q

the liver contains glycerol kinase, what does this enzyme do

A

phosphorylate glycerol and produce glycerol-3-phospahte

151
Q

in glycerol, position 2 has what kind of fatty acid

A

unsaturated

152
Q

what process is used by adipocytes to form TAGs

A

Glyceroneogenesis

153
Q

what stimulates lipolysis

A

glucagon & EPI

154
Q

during lipolysis what is inhibited

A

glycolysis

155
Q

Glyceroneogenesis is essentially an abbreviated version of

A

gluconeogenesis

156
Q

glycerol 3-phosphate is needed for synthesis of

A

triacylglycerol

157
Q

draw pathway for Glyceroneogenesis

A

pg 29

158
Q

about 75% of FA released by lipolysis, what happens to it

A

resterfied to reform TAGs instead of being used for fuel

159
Q

what regulates the levels of PEP carboxykinase

A

cortisol

160
Q

how does liver send TAG to blood?

A

in VLDL

161
Q

what is the “Leash” of FA release

A

insulin

162
Q

if insulin is weak or not working correctly what hapens to FA release

A

insulin is the “leash” so glucagon has a higher role and FA is released at higher rate/amount

163
Q

what does FOX01 do

A

TF that controls gluconeogenesis in genes

164
Q

what is the result of insulin on SREBP’s

A

insulin activates them - they are very sensitive to insulin

165
Q

draw the pathway of insulin affect on SREBP-1c

A

bottom right pg 31

166
Q

draw the effect of insulin and glucose on different TF

A

pg 31 left side

167
Q

describe how hyperinsulemia precedes diabetes

A

an obese person before they are diabetic will have increased insulin resistance. this will continue until eventually their pancreas cannot keep up with demand, and then insulin levels will drop and they will have hyperglycemia

168
Q

what does insulin do to activate glycogen synthesis

A

it activates glycogen synthase via Akt2

169
Q

what does insulin do to decrease gluconeogenesis?

A

inactivates FOX01

170
Q

what promotes activation of SREBP1

A

insulin signaling

171
Q

what activates ChREBP

A

liver when metabolized

172
Q

SREBP1 and ChREBP both promote

A

de novo lypogenesis

173
Q

what does insulin do to adipose tissue

A

inhibits lipolysis & promotes glucose uptake

174
Q

if there is more glucose entering the cell what pathway will be increased

A

PPP

175
Q

If PPP pathway is increased (too much glucose entering) then what is there increased levels of

A

xylulose-5-phosphate

176
Q

xylulose-5-phosphate does what to ChREBP

A

it activates PP2Aδ which will then remove the inhibitory phosphorylations on ChREBP in cytosol and nucleus

177
Q

ativation of LXRα results in

A

increased expression of ChREBP in liver

178
Q

draw out ChREBP pathway and its role in lipid & glucose homeostasis

A

pg 34

179
Q

draw out and explain the main mechanisms of insulin resistance

A

pg 35

180
Q

Increased intracellular diacyglycerols lead to activation of

A

PKC-θ and PKC-ε in skeletal muscle and liver (respectively)

181
Q

activation of PKC-θ in muscle will lead to

A

decreased muscle glycogen synthesis, owing to reduced insulin-stimulated GLUT4 translocation to the plasma membrane.
GLUT4 won’t work as well so more glucose in blooddraw

182
Q

activation of PKC-ε in liver will lead to

A

decreased hepatic glycogen synthesis, owing to decreased activation of glycogen synthase, and increased hepatic gluconeogenesis

183
Q

draw out basic cellular insulin resistance in muscle

A

pg 36

184
Q

draw out basic cellular insulin resistance in liver

A

pg 36

185
Q

draw insulin receptor with insulin sensitivy and insulin resistant

A

pg 37

186
Q

draw insulin receptor pathway

A

pg 37

187
Q

draw insulin sensitive liver

A

pg 38

188
Q

draw insulin resistant/type II diabetes liver

A

pg 38

189
Q

draw prediabetes liver

A

pg 38

190
Q

draw type II diabetes liver

A

pg 38

191
Q

review concept key

A

pg 39

MCB II Block 3 (6 decks)

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