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Biochemistry 2 > fat synthesis > Flashcards

fat synthesis Flashcards

1
Q

3 questions to ask

A

do you have enough energy
do you have enough stored carbs
what should i do now

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2
Q

Fatty acid synthesis

A

you build fatty acids when you consume excess carbs

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3
Q

when dont you build fatty acids

A

when you consume excess fats

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4
Q

how does glucose get in the cell

A

it does not diffuse in the cell directly

2 transport mechanisms

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5
Q

what are the 2 transport mechanisms for getting glucose into the cell

A

sodium independently facilitated transport system

sodium monosaccharide co transport system

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6
Q

sodium independently facilitated transport system

A

glucose transporters GLUT

moves down the concentration gradient

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7
Q

sodium monosaccharide co transport system

A

ATP dependent
transports glucose AGAINST concentration gradient
epithelial cells of intestine, renal tubules and choroid plexus

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8
Q

What are two glucose transport proteins

A

GLUT 2

GLUT 4

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9
Q

glucose galactose and fructose
dietary glucose- out of the intestine (into the blood)
into the liver, kidney, pancreas B-cells
insulin independent

A

GLUT 2

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10
Q

glucose into muscle and adipose tissue
stimulated by insulin
stimulated by low energy charge (AMPkinase)
facilitated diffusion

A

GLUT 4

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11
Q

what are glucose transport statistics

A

in the absense of insulin only 5% of the total transporter pool is found on the cell surface
exercise or insulin result in a 10fold increase in glucose uptake in skeletal muscle
about 90% of insulin stimulated glucose uptake occurs in skeletal muslce
adipose tissue only accounts for 10% of insulin stimulated glucose uptake

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12
Q

what does exercise increase the number of

A

increases the number of GLUT 4 proteins in skeletal muscle

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13
Q

what does exercise stimulate the accumulation of

A

GLUT 4 in the cell membrane for 1-2 hours after exercise

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14
Q

what happens when adding a phosphate to glucose do

A

the glucose concentration in muscle remains low and glucose keeps coming

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15
Q

where is glucose

A

in the blood

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16
Q

what happens when muscle energy is low

A

glucose 6 phosphate runs through glycolysis prep step and krebs to make ATP

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17
Q

what happens when glycogen is low

A

glucose 6 phosphate is converted to glycogen

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18
Q

eating carbs does what

A

elevates blood glucose

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19
Q

when having a elevated blood glucose what happens

A

elevated insulin is caused

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20
Q

what happens with a elevated insulin

A

fat and muscle glucose transport

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21
Q

is the muscle full of glycogen after fat and muscle glucose transport

A

NO glucose is stored as glycogen

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22
Q

is the muscle full of glycogen after fat and muscle glucose transport

A

YES glucose goes to the liver

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23
Q

how does glucose enter the muscle

A

via facilitated diffusion

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24
Q

what does high energy and plenty of glycogen stores inhibit

A

PFK

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25
Q

when PFK is inhibited what does it cuase glucose 6 phosphate to do

A

accumulate and inhibit hexokinase

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26
Q

what does higher glucose concentration in muscle inhibit

A

inhibits facilitated diffusion of glucose

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27
Q

glucose goes to the liver

A

glucokinase

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28
Q

glucokinase

A

lower affinity
stimulated by insulin
not inhibited by product

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29
Q

glucokinase does what

A

runs glycolysis

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30
Q

glycolysis runs for

A

energy and raw material

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31
Q

glucose goes to the liver ultimately for

A

fat building

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32
Q

glucokinase

A

lesser affinity for glucose
not inhibited by its product
stimulated by insulin
stimulated by fructose

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33
Q

what does a increase of glucose satisfy

A

satisfies the low affinity of glucokinase

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34
Q

what is the liver a primary site for

A

for fructose metabolism

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35
Q

what does the liver express

A

frutokinase and triokinase

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36
Q

what does fructose stimulate

A

stimulates glucokinase

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37
Q

what is the liver a primary site for

A

fructose disposal

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38
Q

what are the enzymes essential for fructose metabolism and are highly expressed in the liver

A

fructokinase
triokinase
limited expression in muscle and adipose tissue

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39
Q

where is the fructose 1 phosphate pathway

A

in the liver

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40
Q

what is the entry point into glycolysis

A

glyceraldehyde 3 phosphate

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41
Q

what does a low dose of fructose cause

A

causes a 3fold increase in net liver glycogen synthesis

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42
Q

what do smaller amounts of fructose cause

A

causes the release of glucokinase from a regulatory protein

43
Q

what does not inhibit glucose 6P

A

glucokinase

44
Q

acetyl CoA to

A

FAT

45
Q

where does fructose enter at

A

DHAP G3P

46
Q

what does F6P normally binds to the regulatory protein and what is inhibited

A

glucokinase

47
Q

F1P binds to the regulatory protein and GK is

A

set free and activated

48
Q

fructose and fat the liver preferentially takes

A

in fructose

49
Q

the liver has more what

A

fructokinase and triokinase enzymes

50
Q

what does fructose stimulate

A

GK

51
Q

what does fructose and fat produce

A

more acetyl CoA and ATP

building blocks and energy for building fatty acids

52
Q

excess carbs and protein in the diet do what

A

synthesize FA

store as TAG

53
Q

where is the pathway primarily

A

LIVER
lactating mammary glands
adipose tissue

54
Q

what is the FA synthesis location

A

cytosol Beta oxidation

55
Q

Building fat

A

Eating carbs raise blood glucose
insulin is secreted
glucose enters the cells

56
Q

energy requiring

A

ATP

57
Q

reduced conenzyme

A

nicotinamide adenine dinucleotide P (NADPH)

58
Q

acetyl CoA supplies

A

carbons for the FA chain
glycolysis>pyruvate>acetly CoA
AA catabolism

59
Q

Acetyl CoA needs to get to the matrix to the cytosol is a

A

problem

60
Q

high sugar intake increases what

A

ATP production

61
Q

what can the acetyl portion of acetyl CoA can be transported as

A

citrate into the cytosol

62
Q

why do we need high energy

A

to build fat

63
Q

citrate is where

A

in the inner mitochondrial membrane

64
Q

citrate to acetyl CoA by

A

ATP added to ADP+Pi
citrate lyase
CoA added

65
Q

carboxylation of acetyl CoA

A

acetyl CoA to malonyl CoA y acetyl CoA carboxylase coenzyme biotin

66
Q

malonyl CoA inhibits what

A

CPT I and fat burning

67
Q

what does the reaction of acetyl CoA and Malonyl CoA also require

A

CO2

ATP

68
Q

synthesis of malonyl CoA

A

acetyl CoA to Malonyl CoA by acetyl CoA carboxylase conenzyme biotin

69
Q

what is the rate limiting and regulatory step of FA synthesis

A

acetyl CoA carboxylase ACC

70
Q

Short term regulation of ACC inactive is a what

A

a protomer=subunit

polymerization= combining subunits

71
Q

what is short term regulation of ACC activated by

A

citrate

72
Q

what is short term regulation inactivated by

A

long chain fatty acyl CoA

end product=depolymerization

73
Q

acetyl CoA carboxylase regulation is stimulated by

A

citrate

insulin

74
Q

acetyl CoA carboxylase regulation is inhibited by

A

malonyl CoA
palmitate-end product
epineprine
glucagon

75
Q

metformin and type 2 diabetes

A

inhibtion of ACC
activates AMPK
inhibits ACC and fatty acid synthase
lowers blood glucose

76
Q

the reaction all part of fatty acid synthase the next four steps

A

condensation
reduction
dehydration
reduction

77
Q

condensation is Acetyl ACP and Malonyl ACP to?

A

Acetoacetyl ACP by beta ketoacyl ACP synthase

78
Q

REduction Acetoacetyl ACP to D 3 hydroxybutyryl ACP by

A

beta ketoacyl ACP reductase

79
Q

synthesis

A 
cytosol
acyl carrier protein
adding 2 carbon units
malonyl ACP
NADPH
consuming ATP
80
Q

degradtion

A 
Mitochondria
Coenzyme A
donating 2 carbons units
acetyl CoA
NADH
FADH2
Making ATP
81
Q

conditions that stimulate

A 
high energy charge
increased acetyl CoA
increased NADH and FADH2
increased citrate
increased sugar (glucose fructose)
insulin
82
Q

key enzymes

A

citrate lyase
acetyl CoA carboxylase
fatty acid syntase CRDR

83
Q

TAG synthesis in the what

A

mitochondria

84
Q

elongation is accomplished through

A

elongases and requires NADPH

85
Q

desaturation is accomplished through

A

desaturates by adding double bonds

86
Q

what are separate enzymatic processes

A

mitochondria

smooth ER

87
Q

what can humans not create

A

double bonds beyond the 9-10th carbon

88
Q

NADPH where does it come from

A

pentose phosphate pathway

malate-pyruvate in cytosol

89
Q

NADPH source of electrons in?

A

synthesis

90
Q

Fatty acids are what kind of molecules

A

highly reduced

remember reduction is gain of hydrogen and electrons

91
Q

dehydraton D3 hydroxybutryrl ACP to Crotonyl ACP

A

by beta hydroxyacyl ACP dehydratase remove H2O

92
Q

reduction 2 by Crotonyl ACP to Butyryl ACP by

A

Enoyl ACP reductase

93
Q

Palmitate (16:0) when does this process stop

A

when we have 16 carbon palmiate

94
Q

fatty acid synthesis

A

reduction
dehydration
reduction

95
Q

fatty acid synthase

A 
CRDR
Condenses-adds molonyl CoA
Reduces- with NADPH 
Dehydratase
Reduces- with NADPH
96
Q

release the fatty acid

A

palmitoyl thioesterase
last step of FAS
cleaves thioester bond and releases saturates palmitate

97
Q 
Update:
Butyryl
last 3 carbons are?
still attached to?
Transfer the butyryl chain to the what site?
add another?
when does growth stop
A 
(4 carbons)
hydrogen saturated
ACP
holding site (cysteine)
add malonyl CoA and repeat
at 16 carbons of palmitate
98
Q

long term regulation ACC

high calorie/high carb diet

A

increase ACC synthesis which increase FA synthesis

99
Q

long term regulation ACC

low calorie/ high fat diet

A

decrease ACC synthesis which decreases FA synthesis

100
Q

long term regulation ACC

upregulated by insulin

A

increased response/increased receptors

increase ACC synthesis which increase FA synthesis

101
Q

multi enzyme complex is

A

FA synthesis

one portion of the molecule is ACP

102
Q

one portion of the molecule is ACP

A

acyl carrier protein ACP
similar to coenzyme A
terminal thiol group at the end of an arm

103
Q

short term regulation of ACC

reversible phosphorylation

A

AMP- activated protein kinase AMPK- phosphorylates and inactivates ACC

104
Q

short term regulation of ACC

reversible phosphorylation

A

can be activated by cAMP dependent PKA
epinephrine and glucagon increase cAMP which phosphorylates and inactivates ACC
insulin dephosphorylates and activates ACC

Biochemistry 2 (13 decks)

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